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Immunology Introduction - Innate vs. Adaptive -Humoral vs. Cellular - Complement - Hypersensitivity — Transcript

by Medicosis Perfectionalis · 10,378 words · 1,601 segments · language en · Watch on YouTube

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0:00What is going on wonderful people? It's
0:02Medicosis Perfectionis where medicine
0:04makes perfect sense. Welcome to my
0:06immunology playlist. In this playlist,
0:09you will learn about the bone marrow
0:11which is the source of all of your blood
0:13cells including red blood cells, white
0:16blood cells, and platelets. When it
0:18comes to the immune system, do we care
0:20about red blood cells? The answer is no.
0:22Do we care about platelets? The answer
0:24is no. But do we care about the white
0:26blood cells? The answer is absolutely
0:29yes. The white blood cells form your
0:32army that will defend you against
0:34foreign invaders whether they are
0:37bacteria, viruses, fungi or otherwise.
0:40And if that was not enough, your immune
0:43system, particularly the Tlymphosy, can
0:46help you fight cancer cells, which means
0:49the stronger your immune system, the
0:52less likely you are to develop cancer.
0:54Conversely, the weaker your immune
0:57system, the more vulnerable you are to
0:59cancers. Click the like button, click
1:02the subscribe button, and let's get
1:04started. Today, you're going to learn
1:06about blood plasma, plasma proteins,
1:10antibodies, also known as
1:11imunoglobulins, otherwise known as gamma
1:14globbulins, blood cells such as the red
1:17blood cells, the white blood cells, and
1:19the platelets. First, let's talk about
1:20your blood. Your blood is made of plasma
1:23and cells. The plasma is made of water
1:25and electrolytes and plasma proteins.
1:28The plasma proteins include albammen and
1:32globulins. Globulins are many including
1:35alpha globulins, beta globulins and
1:38guess what? Gamag globbulins. As for the
1:41blood cells, they are the red blood
1:42cells, the white blood cells, and the
1:45platelets. When it comes to the immune
1:47system, we care about the white blood
1:49cells. But if you do care about the red
1:51blood cells and the platelets, then go
1:53watch my hematology playlist and my
1:56bleeding and coagulation playlist.
1:58Today's video is an introduction to
2:01immunology just like my video on
2:03introduction to hematology. I have an
2:05introduction video to every subject and
2:08system. Let's talk about the plasma. The
2:11plasma is made of water and electrolytes
2:14and plasma proteins. Water is 90% of the
2:18plasma and the plasma is about 55% of
2:21the whole blood. How much blood do you
2:24have? About 5 lers. The electrolytes
2:27include kines and annions. Kines such as
2:31sodium, potassium, calcium, magnesium,
2:33annions or negatively charged
2:35electrolytes such as chloride,
2:37bicarbonate, phosphate, sulfate, etc.
2:39Please say chloride not chlorine.
2:42Chlorine is a poison. Your body does not
2:45have chlorine, but your body has
2:48chloride. Careful because medical
2:51textbooks are the only type of books
2:53that can kill you from a typo. Pay very
2:56close attention when you read and when
2:58you write. What's the major cation in
3:00the plasma? Sodium. And the major anion
3:03chloride. Positive charge, negative
3:05charge. And that's why sodium and
3:07chloride love to follow one another
3:10because opposites attract. just like all
3:13your previous relationships. How did
3:15that work out for you? Plasma proteins
3:17include albamine and globulins and then
3:20you have a bunch of lipids,
3:21lipoproteins, etc. And don't forget some
3:25gases are soluble on your plasma and
3:27other gases are bound to the hemoglobin.
3:30So there is oxygen that is soluble in
3:32the plasma and oxygen that's bound to
3:35the hemoglobin. We call that
3:36caroxyhemoglobin.
3:38Similarly, there is carbon dioxide
3:40floating freely in your plasma and there
3:43is carbon dioxide bound to the
3:45hemoglobin. We call that carbamino
3:48heemoglobin, not caroxyhemoglobin.
3:51Caroxyhemoglobin is a poison just like
3:54chlorine. You should not have
3:55caroxyhemoglobin in your body.
3:58Caroxyhemoglobin means that your
4:00hemoglobin is bound to carbon monoxide,
4:04not carbon dioxide. So if your
4:06hemoglobin is bound to carbon dioxide
4:09which is normal this is called carbamino
4:11hemoglobin. But when your hemoglobin is
4:14bound to carbon monoxide which is
4:16abnormal this is called
4:18caroxyhemoglobin.
4:20See my video on carbon monoxide
4:22poisoning and the story of the young lad
4:25in the garage. Plasma proteins can be
4:27divided into two main groups. Albamine
4:30and globulins. Which one is more
4:32abundant? Albine of course. It's about 4
4:34g per deciliter. A desi of anything is
4:381/10enth of that thing. So decile liter
4:42is 1 tenth of a liter. Put differently,
4:45one liter equals 10 des. A desi is a
4:50tenth of anything. What is a desi
4:53millionaire? Oh, this is someone with a
4:56net worth of 110th of a million, i.e. a
5:00100,000. How about centi? Centi as in
5:03centimeter is 1 100th of that thing. So
5:07centimeter is 1/100th of a meter. Put
5:10differently 1 meter contains 100 cm. So
5:15what is a centmillionaire?
5:17That is someone with a net worth of
5:2010,000. Please do not confuse desi with
5:24deca. Desi means one10enth. Deca means
5:2810. So a deca millionaire is someone
5:32with a net worth of 10 million dollars
5:35or euros or pounds or what have you.
5:38Desi is not the same as deca. Globulins
5:40are many including alpha, beta and gamma
5:43globulins. Globulins include
5:45fibbrrenogen which is coagulation factor
5:48number one and proth thrombin which is
5:50coagulation factor number two. If you
5:53wish to see more videos like this in the
5:55future, drop a test tube emoji in the
5:58comments. Question: What do you call a
6:01test tube that has completed its
6:03education? Answer: a graduated cylinder.
6:08Globulins are many such as alpha 1
6:10globulins, alpha 2 globulins, beta
6:12globulins, and gamma globulins. Alpha 1
6:15globulins are many. Here is just one
6:17example, the alpha 1 antitrepin. How
6:20about alpha 2 globulins? There are many
6:22of them such as andutenogen
6:25betaglobulins there are many of them
6:27such as transferin which transfers iron
6:30feric ferrus this is iron and that's why
6:34in the periodic table of the elements
6:36the symbol for iron is fee it's from
6:39this origin when something ends in I in
6:42it's usually a protein oh such as
6:45transferin such as globulin such as
6:48antitripen we get this from the word
6:51protein itself self which also ends in I
6:53in N. The more you know. How about
6:55gamaglobulins? These are aminoglobulins.
6:59Notice the in also known as antibodies.
7:02There is the body and there is the
7:04antibbody. Just like there is trison and
7:07there is anti-tripen. There is clockwise
7:10and anticlockwise. There is matter and
7:14antimatter. Don't get me started on
7:17modern physics because it has become
7:19another metaphysics. If you wish to
7:22download these colorful notes, go to
7:24medicosisperfictionalis.com.
7:26I help you learn, understand, and pass
7:28exams. If you want me to personally
7:30tutor you, reach out to me on my
7:32website. Let's talk about blood cells
7:34and antibodies. Here is your bone
7:36marrow. It has stem cells, particularly
7:39pur potent stem cells. To learn about
7:42the different types of stem cells,
7:44please refer to my video titled stem
7:46cells in my biology playlist. The purip
7:49potent stem cells of the bone marrow are
7:52divided into the myoid stem cells and
7:54the lymphoid stem cells. This is called
7:57the myoid lineage. This is the lymphoid
8:00lineage. Myoid cells will give you
8:02proariththoblast, ereiththroblast
8:04whatever whatever whatever until you get
8:06the mature urethraite which is the red
8:09blood cell. Then the myoid cells will
8:11give you meggaaroblast which will become
8:13yada yada yada megaarioite. The
8:15meggaarioite is a big cell. It will
8:18literally explode into thousands of
8:21pieces. Each piece is a platelet. We
8:24also have myoblasts which will give you
8:27these granulosytes. What are the
8:29granulosytes? The acronym is ben
8:32basophils. Eocinophils neutrfils.
8:34Basopils have basophilic granules.
8:37Eocinophils have eosinophilic granules.
8:40Neutrifils have neutral granules that
8:43are neither acidic nor basic. Neither
8:45basophilic nor eosinophilic. Myoid will
8:48give you monoblasts which will
8:49eventually become monocytes. These have
8:52the same origin as your macrofase
8:55and keep this in mind because the
8:57macrofase will play a very important
8:59role in the immune system. All of that
9:02was myoid. But how about the lymphoid?
9:05Lympoid cells will give you
9:06lymphoblasts. Lymphoblasts will give you
9:08lymphocytes. What kind of lymphocytes do
9:11we have? We have Blymphosytes and we
9:13have Tlymphocytes. They also give us
9:15natural killer cells. These are street
9:17fighters. They are not specific. They
9:19just punch everyone in the face. But
9:22your military is very specific because
9:25it has an army. It has the navy, the air
9:28force, space force, the marines, etc.
9:31The betosytes will become plasma cells.
9:33The plasma cells will make antibodies,
9:36also known as amunoglobulins, otherwise
9:38known as gamma globulins. If you want to
9:41boost the production of red blood cells
9:43from the bone marrow, EPO is your
9:46friend. If you want to boost the
9:47granulosite formation by the bone
9:50marrow, you need to talk to granulosite
9:52colony stimulating factor. To boost the
9:55production of monocytes from the bone
9:57marrow, MCSF is your guy. This is monocy
10:01colony stimulating factor. To boost the
10:04production of platelets from the marrow,
10:06you need to talk to thrombopetin. Who
10:09makes epo your kidneys? Who makes your
10:12liver? I've talked about each one of
10:14them in its own video in my hematology
10:17playlist. The white blood cells are many
10:19including eosinaphils, neutrfils,
10:21basophils, lymphocytes, monocytes. You
10:24can also add natural killer cells. Then
10:27are the granulosytes. The basophils,
10:29eosinaphils, neutrfils. How about the
10:31lymphocytes and the monocytes and the
10:33natural killer cells? They are non
10:35granulosytes. There is a condition known
10:37as a granulocytosis in medicine. What
10:40does that even mean? Osis means
10:42condition just like the name of my
10:44channel. It's medicosis perfectionis a
10:47condition of perfect medicine.
10:49Granulosite. Granular cell. What are the
10:52granulosytes? These are the cells that
10:55have the granules such as basopils,
10:57einophils, neutrfils and a means no as
11:00in atom atypical etc. So put together a
11:04granuloccytosis means it's a condition
11:08where your body does not have enough
11:11granulosytes
11:12i.e. your body lacks the neutrfils,
11:15basophils and eucinophils. Is this a bad
11:17thing? It's a horrible thing because
11:20without the granulites you'll have hard
11:22time fighting infections and you'll have
11:25increased risk of infections. If your
11:27military is a joke, you're more likely
11:30to get invaded. Which reminds me of what
11:33will Durand said, quote, "Nations should
11:36call for peace while keeping their
11:39powder dry." What is the normal total
11:42white blood cell count in your blood? It
11:44should be between 4,000 and 11,000 white
11:48blood cells per microl of blood. For the
11:51pros, microl is the same exact thing as
11:56cubic millm. They are absolutely
11:59equivalent. So if I say that my total
12:02lucitic count is 5,000 cells per microl,
12:07it's the exact same thing as saying
12:09there are 5,000 cells per cubic millm.
12:13If you take it up a notch, you will find
12:16that milll is the exact same thing as
12:19cubic cm, which you call cubic cm or cc.
12:24So, if I say that the engine of my car
12:26has a capacity of 2,000 cc's, it means
12:312,000 cm, which means 2,000 ml, which
12:36means it's a 2 L engine. And if it was
12:39made in Japan before 2018, you probably
12:43have a very good engine. If it's made by
12:45any other country, it's probably a piece
12:47of junk. Sorry, got excited. Assume that
12:51my total luccoitic count lucco means
12:54white site means cell. So luccoite means
12:57white blood cell is 5,000. That's my
13:00total white blood cell count or total
13:02luccoitic count. Neutrifils should make
13:0560% of the total white blood cell count.
13:08That's the relative neutrfilic count.
13:11What if you want the absolute neutrfil
13:13account? You simply multiply 60% by
13:165,000. you get 3,000
13:203,000 neutrfils per microl of blood.
13:24That's your absolute neutrfilic count.
13:27If you want for the lymphocytes, you
13:29multiply 30% by 5,000. And this will
13:32give you 1,500 lymphocytes per microl or
13:37per cubic millm of blood. And you do the
13:41same thing for monocytes, einophils, and
13:43basopils. This is relative count. This
13:46is absolute count. This is the total
13:49luccoitic count. When you multiply the
13:52relative by the total, you get the
13:54absolute white blood cells. That's your
13:56army. What's the function of the
13:58neutrfils or the polymorphonuclear
14:00luccoytes? They fight bacteria. They
14:03make pus. The pus cells are the
14:06neutrfils. Apsis is a collection of pus.
14:09Impaema is a collection of pus. They do
14:11have neutrfils. Neutrfils are the heroes
14:14of acute inflammation. How about
14:16lymphocytes? Those are the heroes of
14:18chronic inflammation. They fight viruses
14:21and fungi. They help you make a
14:23granuloma. In the good old days, we used
14:26to call that a tuberculo. And that's why
14:28the bacteria that cause tuberculosis,
14:31i.e. the miccoacterium tuberculosis, was
14:34known in the past as the tubercal
14:36basilli. Why do you call it tubercal?
14:39Because it forms a granuloma. Why do you
14:42call them basilli? Because they look
14:44like this. They look like this under the
14:46microscope. They look like rods and not
14:48spheres. Lymphocytes are the cells of
14:51adaptive immunity or acquired immunity.
14:54More on that later. They also help you
14:56in type four hyper sensitivity
14:58reactions. More on that later.
15:01Monocytes, they become macrofasages.
15:03When they are in the blood, we call them
15:05monocytes. When they go to the tissue,
15:07we call them macrofasages. Macrofasages
15:10are fagocitic cells. They love to eat
15:12foreign invaders. They will also help
15:15you make a granuloma. Next, eocinophils.
15:18When it comes to the eocinophils, just
15:21say ew. Just like the meme. What's the
15:24function of eocinophils? Just say ew.
15:27Allergy. Ew. Anaphilaxis. Ew. Parasites
15:32double triple. Ew. Basopils make
15:35histamine. Basophils and mass cells are
15:38similar but not the same. They have
15:40different lineage. But monocytes and
15:42macrofasages are kind of the same. The
15:45difference is monocytes are in the
15:46blood. Macrofasages are in the tissue.
15:48You can also call them hysteocytes, the
15:50cells of the tissue. Histologology is
15:53the scientific study of the tissue. And
15:55no, I'm not referring to the tissue that
15:58you sneeze in. I mean the tissue as in a
16:01collection of cells. Macrofasages and
16:03monocytes are also the equivalent of cup
16:06for cells in the liver. So when they are
16:08in the blood, they are monocytes. When
16:10they go to the tissue, they are
16:12macrofasages. When they are in the
16:13liver, they are cup for cells. When they
16:15are in the nervous system, they are
16:17microglea. When they are in the bones,
16:19they are the osteoclast. They're always
16:21eating stuff. Osteoclasts will eat the
16:24bone. They will chew away the bone.
16:26Microglea will eat the foreign invaders
16:29that try to invade your brain. Cup for
16:31cells. Same thing, but for the liver.
16:34These are your blood cells. Pause and
16:36review. What are the cells of acute
16:38inflammation? The heroes of acute
16:40inflammation are the neutrfils. These
16:41are polymorphonuclear cells or PMNs for
16:45short. Chronic inflammation. Who are the
16:48heroes? Lymphocytes. These are monuclear
16:51cells. Why? Because the neutrfils have
16:53different shapes for the nuclei. The
16:55PMNs are not just neutrfils. They're
16:57neutrfils and others. And they have
16:59different shapes in the nucleus. For
17:01example, the neutrfll has the segmented
17:03nucleus. It could have three segments or
17:05four segments or five segments. More
17:07than that is a disease. It's hyper
17:10segmented neutrfll seen in cases of
17:13megaloblastic anemia. But lymphocytes
17:16well they have the same shape of a
17:18nucleus. The nucleus always looks like a
17:20pie or a pizza. It occupies most of the
17:23cell and that's why it's just one shape
17:26monuclear and it's definitely one piece.
17:29But this neutrfil has multiple pieces
17:31polymorphonuclear.
17:32Here are the squle of acute inflammation
17:35and the consequences of chronic
17:37inflammation. Note that chronic
17:39inflammation can lead to cancer in some
17:42cases. So hepatitis B virus and
17:45hepatitis C virus can lead to chronic
17:47inflammation of the liver or chronic
17:49hepatitis. This can become liver cancer
17:51or hepatellular carcinoma in the future.
17:55H pylori can lead to chronic gastritis,
17:57chronic inflammation of the stomach, and
18:00this can lead to gastric cancer. Chronic
18:03inflammation is no joke. I've talked
18:06about acute versus chronic inflammation
18:08in great detail in my pathology
18:10playlist. Now, let's talk about your
18:12immune system. Natural versus acquired,
18:15innate versus adaptive. The immune
18:18system is divided into innate or natural
18:21immunity and adaptive or acquired
18:23immunity. Innate or natural immunity,
18:26you were born with it. You did not do
18:29anything to acquire it. But when it
18:31comes to the adaptive or the acquired
18:33immunity, you have to learn it. You have
18:36to work hard for it. It is not given to
18:39you. The natural immunity is given to
18:42you. It's innate. It's not specific.
18:44It's less potent. It's present at birth.
18:46It has no memory. It cannot remember
18:48previous infections and it responds to
18:50foreign invaders in the same manner. For
18:53example, the acid in your stomach is an
18:55example of the innate immunity. Do you
18:57think the acid of the stomach cares
18:59whether the invader is a bacterium, a
19:01virus, a fungus, or a parasite? The
19:04answer is no. It's an acid. It doesn't
19:06care. It cannot adapt. However, your
19:09adaptive or acquired immunity is very
19:11specific. For example, you have some
19:13cells that only fight stafloccus orius,
19:16which is only one type of bacteria, and
19:18other cells that fight staflloccus
19:21epidermis, which is still a staff, but a
19:24different type of stafloccus, a
19:26different species of stafloccus. So, you
19:29need another cell for it. Very specific,
19:31very specialized, just like your
19:33military. Are we born that picky and
19:36that specific? No. You have to develop
19:38this by trial and error. You get exposed
19:42to a certain invader, you fight it so
19:45you learn from your mistakes so that
19:47your next attack is going to be stronger
19:50and faster. The innate immunity is not
19:53specific, meaning it cannot recognize
19:56specific antigens. Its innate, i.e. does
19:59not require previous exposure. It's a
20:02very rapid response, but it's less
20:04efficient when you compare it to the
20:06adaptive immunity. Examples of innate
20:08immunity, mechanical barriers like your
20:10skin, chemical barriers such as the acid
20:13in the stomach, the mucus on your mucous
20:15membranes and your epithelium,
20:17non-specific cellular defense,
20:19microfasages and macrofasages. What the
20:22hell is a microfage? Neutrfils and
20:24eucosinophils because they are tiny but
20:26the macrofase is huge. And natural
20:28killer cells. These are street fighters.
20:30Not specific. also non-specific hemoral
20:33defenses. The lossomes, the interferons,
20:36the acute phase reactants, they just
20:38destroy almost everything in front of
20:40them. They don't care. They cannot
20:42differentiate or distinguish. The innate
20:45immunity is the acid in your stomach,
20:47the psyia in your trachea, the IgA in
20:51your saliva, in your oral cavity, in
20:53your nasal cavity, in vaginal canal,
20:56anal canal, any mucous membrane. Your
20:59skin is a barrier. So that's innate. But
21:02the adaptive or the acquired immunity is
21:05different. And we can divide that into
21:07naturally acquired. It's not your
21:10doctor's fault versus artificially
21:12acquired. It is your doctor's fault or
21:15virtue. Naturally acquired had nothing
21:17to do with the doctor. For example, you
21:19came out of your mother's womb with some
21:22antibodies that you got from your
21:24mother. This is passive. You did not do
21:26anything to earn it. Moreover, your
21:28mother breastfed you, giving you more
21:31antibodies with the milk. Still, you
21:34were passive. You did not do anything to
21:36acquire. Your mother did the heavy
21:39lifting for you. She developed the
21:42antibodies on her own and then gave you
21:45preformed antibodies. versus when you
21:48actually have an infection, an infection
21:51that affects you. Then you fight the
21:54infection, fight the infection, fight
21:56and win. Now you were active. You
21:59actually did something to earn it. Did
22:01the doctor have anything to do with the
22:03infection or the breastfeeding or the
22:05birth? No. These are natural processes.
22:08What your doctor can do, artificially
22:11acquired adaptive immunity, is to give
22:14you an anti- serum or to give you a
22:16vaccine. If the doctor gives you an
22:18anti-erum, you are passive in that
22:20regard. Why? An anti- serum is something
22:23that you get from the plasma of another
22:25patient who was infected before, made
22:29antibodies before, and then you take
22:32those antibodies in order to fight your
22:35infection, to fight your battle. So, you
22:38did not do anything. You just borrowed
22:41the weapons made by another person. But
22:44when the doctor gives you a vaccine,
22:46let's imagine it's a live attenuated
22:48vaccine, then the doctor give you a
22:51weakened form of a virus or a bacterium
22:54and then you have to fight this virus or
22:57this bacterium. Then you develop an
23:00immune response. So you are active in
23:03that regard. When the lymphocytes start
23:06early on, they are naive. They are not
23:08mature. They are not trained yet. Once
23:12they recognize the antigen, i.e. a piece
23:14of the foreign invader, be it bacteria,
23:17fungus or virus, then your lymphocytes
23:20will grow the hell up and mature and
23:23they will remember the previous fight.
23:26So that if we encounter the same
23:28organism in the future, the second
23:30response is going to be stronger and
23:32faster. And that's why when I make fun
23:34of my students, I usually tell them,
23:37hey, you're as naive as the bilymphosy
23:40before it recognized the antigen. Let's
23:42focus on the antibodies, also known as
23:45amunoglobulins or gamma globulins.
23:48Antibodies only come from the plasma
23:50cells, which only come from the
23:52Blymphosytes, not the Tlymphosytes. How
23:55many types of antibodies do we have? The
23:57answer is we have five. IgM, IgA, Ig,
24:01Ign.
24:02This classification is based on their
24:05heavy chains such as this and that. But
24:08how about the light chains? The light
24:11chains could be kappa or lambda. So you
24:14can have an antibbody that is IgM lambda
24:16or IGM kappa. Ig kappa or Iga lambda etc
24:22etc etc. You mix and match. IGM IG A IG
24:26G I G E or IG D. The acronym is Majid
24:30which is an Arabic name. IGG is small,
24:33but IGM is very large. It's the largest.
24:36Because IGM is small, it can cross the
24:38placenta from the mother to the baby and
24:40wreck havoc on the baby in some cases.
24:43And this is the story of RH
24:45incompatibility, which I've talked about
24:48in a separate video. But IGM is very
24:50big, which means it cannot cross the
24:52placenta. IGG is small but very
24:55abundant. It's the highest concentration
24:58compared to any other antibbody. Let's
25:01say that I encounter the same bacterium
25:03twice, two separate infections. In the
25:06first response or the first infection,
25:08it's going to be IgM. Later, the second
25:11response will be via IGG. Primary
25:14response, secondary response. Note that
25:17both IgM and IGG can fix i.e. activate
25:21the complement cascade which we'll talk
25:24about later in this video. IGG has
25:26another function which is opssonization.
25:28What does obsinization mean? To opsinize
25:31is to make something tasty. So when you
25:34obsinize bacteria, you make them tasty
25:37so that your immune cells can enjoy
25:40themselves while eating the foreign
25:42invaders. IgA is the only one that
25:46decides to leave the blood and ascend to
25:48the mucosa or the mucous membrane such
25:51as your nose, your mouth, your fairings,
25:54your larynx, vaginal canal, anal canal,
25:58the mucus surface of the gut, the mucous
26:00surface of the respiratory tract, etc.
26:03IG is produced first as part of the
26:05primary response. The function is not
26:08well known. There are many speculations,
26:10but we do not know for sure. Here's the
26:13antibbody or the amoglobulin or the
26:15gamag globulin. It has two heavy chains
26:18as you see and two light chains. The
26:21dark blue color is the heavy chains. The
26:24light blue color is the light chains.
26:27This is the constant portion of the
26:29antibbody. That's the letter C. And this
26:31is the variable portion of the antibbody
26:33letter V. V subL means it's variable and
26:37light. V subh means variable and heavy.
26:41C sub L is constant and light. C subH is
26:45constant and heavy, constant, heavy,
26:47constant, heavy, etc. Just like your
26:49door, there is a hinge. To keep both
26:52sides together, we have a dulfide bond
26:55between sulvers. The antigen or the
26:57piece of the bacterium or the piece of
26:59the invader is going to bind here. Here
27:02is the antigen or the piece of the
27:04bacterium binding here. This is
27:06variable. This is constant. How about if
27:08I have a cell like a macrofase? It will
27:11bind here. Here's the macrofase binding
27:13to this part of the antibbody. How about
27:15the complement system? Oh, the
27:17compliment proteins will bind here. Why
27:19do we call it complement? Because it
27:22complements the action of the antibbody.
27:24Here's the foreign invader, the
27:26bacterium. You take a piece of it.
27:28That's the antigen. The antigen will
27:31bind the antibbody. They bind together.
27:33This is the antigen antibbody reaction.
27:36Here's the macrofase bound to the base
27:38of this antibbody. constant portion. Of
27:41course, antigen antibbody reaction is
27:43also known as aglutination where the
27:46antigen is the aglutenogen and the
27:49antibbody is the aglutin. Why do you
27:52call it antigen? Because it generates an
27:55antibbody response. That's why we call
27:58it an antigen. Why do you call it
28:00aglutenogen?
28:02Because it generates an agluten against
28:05it. Here is the antigen and the
28:07antibbody bound together in the
28:09aglutination process or the antigen
28:12antibbody complex. The complement can
28:14come to complement the function of the
28:17antibbody. The antigen antibbody complex
28:19is important. The antigen alone not
28:22active. Antibbody alone not active but
28:24the antigen antibbody complex very
28:27active. Active to do what? To neutralize
28:30the foreign invader i.e
28:33rendering it powerless to opsinize the
28:36foreign invader rendering it tasty so
28:39that your immune cells will enjoy
28:41themselves while eating the foreign
28:43invader bonapet antigen antibbody
28:46complex is the story of aglutination see
28:49my hematology playlist and activation of
28:52natural killer cells and activation of
28:55the classical compliment pathway which
28:58we'll talk about at the end of the video
29:00let's summarize immunology in one slide.
29:03I want you to imagine that you are a
29:05customer sitting at a restaurant and
29:08then the waiter comes to you with the
29:10food. The food is presented on a tray.
29:13The waiter is going to present the food
29:16to you and then once you see the food,
29:19you will eat it. You will remember it
29:21and you're more likely to come back to
29:23the restaurant and order again. Your
29:27next order is likely to be more
29:29efficient. Now, what is the food? The
29:31food is the antigen. What's the antigen?
29:33The antigen is a piece of the bacterium
29:36or the virus or the fungus etc. It's a
29:39piece of the foreign invader. Who is the
29:41waiter that presents the food? The
29:43waiter is the antigen presenting cell.
29:46This antigen presenting cell could be a
29:49macrofage, a blymphosy, a dendritic cell
29:53or longer hans cell. And what's the tray
29:56that you use to put the food on? The
29:58answer is it's the MHC major
30:01hystocompatibility
30:02complex. Here we see the waiter
30:04presenting the food on a tray. Here we
30:07see the antigen presenting cell
30:09presenting the antigen on a major
30:12hystocompatibility complex. Presenting
30:15to whom? To the customer i.e. the
30:18lymphocy. Once the lymphocy looks at the
30:21food we have three options. We can eat
30:24it i.e. destroy the microbe, destroy the
30:27foreign invader or we can remember it,
30:30become a memory cell to remember the
30:33next exposure so that the second
30:35exposure is faster and stronger and then
30:37the customer can share the good news
30:39with others. This is the blymphosy
30:42becoming plasma cells and the plasma
30:44cells make antibodies such as IGM, IGA,
30:48IGG, IG and IG. What's an antigen? An
30:52antigen is anything that triggers your
30:54immune system, i.e. it generates an
30:57antibbody. It generates an imunological
30:59reaction. It's a foreign substance that
31:01stimulates your immune system triggering
31:03an immune response. What's a heptin? A
31:06heptin is a baby antigen. It's a very
31:08small molecule on its own is not
31:11sufficient to trigger an immune
31:13response. However, if it binds to a
31:15protein making a heptin protein immune
31:19complex, this is sufficient to trigger
31:21an immune response from you. Let's
31:24compare between belymphosytes and
31:26tlymphosytes. The origin both are made
31:28in the bone marrow by the lympoid stem
31:31cells which come from the purip potent
31:33stem cells. So we start with purip
31:35potent stem cells then lymphoid cells
31:39then lymphoblasts then the lymphocytes
31:42which are belymphosytes and tlymphocytes
31:44that was the origin. How about the site
31:47of maturation where did they go to
31:49school in order to learn the
31:51blymphosytes matured in the bone marrow
31:54whereas the tlymphocytes received their
31:57education in the thymus. For the pros,
31:59the bone marrow is misodermal whereas
32:01the thymus is endodermal in origin. See
32:04my embryology playlist. After they get
32:08educated in school, they go to the real
32:11world. They go to the job site. Where do
32:14they work? The Bymphosytes will work in
32:16the lymph nodes and the spleen. How
32:17about the T- cells? Also in the lymph
32:19nodes and the spleen, but in different
32:21departments. So the B cells will work in
32:24the follicles of the lymph node which is
32:26part of the cortex of the lymph node but
32:29the T- cells will work in the para
32:31cortex of the lymph node. How about in
32:33the spleen? The B cells will work in the
32:36follicles of the spleen part of the
32:38white pulp but the T- cells will work in
32:40the per arterolar lymphatic sheath also
32:43in the white pulp. The white pulp is
32:46part of the spleen because if you
32:48remember the spleen is made of red pulp
32:50and white pulp. The red pulp contains
32:53red blood cells i.e. blood whereas the
32:56white pulp contains white blood cells
32:59such as blymphosytes and tlymphosytes.
33:02Can the bymphosytes make antibodies? The
33:04answer is yes. Can the tymphosytes make
33:07antibodies? The answer is no.
33:09Blymphosytes can become plasma cells and
33:12make antibodies. T- cells do not make
33:14antibodies. When you make antibodies,
33:16they are secreted in the blood or in the
33:19mucous membrane. in your tears, in
33:22vaginal secretions, in the ear wax, in
33:25every part of the body, in every fluid
33:28that you can imagine. Hence the word
33:31humoral. If you remember the ancient
33:34Greeks of antiquity, they had the theory
33:36of the four humors, which were blood,
33:40flem, yellow bile, and black bile. And
33:43they use that theory to explain almost
33:45everything from their ecosystem to human
33:49psychology. So humoral immunity is
33:51called humoral because you're making
33:54antibodies in the fluids of the body.
33:57The belmphosytes do not have to become
33:59plasma cells and make antibodies. They
34:01can also become memory B cells to
34:04remember the next infection so that the
34:07next response is going to be stronger
34:09and faster. But tell me about the
34:11tymphosytes. They do not make
34:14antibodies. So we cannot call that
34:16hemoral immunity. What do they do then?
34:19They punch the fungus in the face. They
34:21punch the cancer in the face. They punch
34:23the virus infected cell in the face. Oh,
34:26it's a facetoface action. It's cellto
34:30cell response. Hence, cellular immunity
34:33or cell mediated immunity. Tly
34:35lymphocytes come in many shapes. You
34:37have the T helper cell and the T-cytoxic
34:40cell. The T helper cell helps everyone.
34:44She's going to help her sister. Her
34:46sister is another Tlymphosy. the T-side
34:49toxic and she's going to help her
34:51neighbor. Her neighbor is the Bly
34:54lymphocy. So her sister is another
34:57Tlymphocite but her neighbor is the
34:59belymphocy. For the pros, when the tea
35:02helper makes TH1, it's going to help the
35:05T-side toxic. Her sister comes first.
35:08After I help my sister, I can help my
35:12neighbor second. So TH2 is going to help
35:15the be lymphocy which means there are
35:18many subtypes of the tea helper such as
35:20TH1 to help her sister and TH2 to help
35:24her neighbor. How about the T cytotoxic?
35:26It's cytotoxic toxic to the cells. What
35:29kind of cells? Fungal cells, cancer
35:32cells, virus infected cells. When a
35:34virus infects one of your cells, your
35:37T-side toxic is going to destroy not
35:40just the virus but the virus and your
35:42cell that swallowed the virus. That is
35:45very cytotoxic. So hemoral immunity
35:48belymphosytes cell mediated immunity
35:50tymphosytes do bymphosytes make
35:52antibodies? Yes, they become plasma
35:54cells and the plasma cells make
35:56antibodies. How about the tymphosytes?
35:58They do not secrete antibodies. They
36:00punch the cell in the face. Cell
36:02mediated hemoral immunity beymphosy. The
36:06bly lymphosy fights bacteria whereas the
36:09tlymphosy fights cancers fungi virus
36:14infected cells. It's also responsible
36:16for rejecting the new organ that the
36:19doctor transplanted in you. Are the
36:22tilymphosytes important? Of course they
36:25are. to belabor the point because it's
36:27worth belaboring. Let me tell you about
36:29two different types of vaccine against
36:32the numoccoal pneumonia. This is
36:34streptococcus pneumonia otherwise known
36:36as the numoccoy. There is the 23 veilent
36:39vaccine known as ppsv23
36:42numoccoal polysaccharide vaccine 23
36:45versus the numokal conjugated vaccine
36:48PCV13 numokcoal vaccine 13 or veent 13.
36:54What's the difference? The PPSV23
36:58does not activate the tymphocy. Why not?
37:02Because it's not bound to a conjugated
37:04protein. It's simply sugar.
37:06Polysaccharide sugar. Just sugar. No
37:09protein. If it's not linked to a
37:11protein, it's not going to activate the
37:13tlymphosytes. Since the tilymphosytes
37:17grow up in the thymus or as my professor
37:20used to say the thymus then this vaccine
37:22is thymus independent not thymus
37:26dependent and if you're not going to
37:28activate the tea cells then the tea
37:30helpers will not activate the
37:32bymphosytes meaning the bymphosytes will
37:35not grow up they will not class switch
37:38they will not make their antibodies they
37:40do not cause a memory response contrast
37:44that with the stronger PCV13.
37:47This is conjugated to a protein. If it's
37:50conjugated to a protein, it's going to
37:53activate the Tlymphosytes, which means
37:56thyos dependent. And the Tlymphosytes
37:59include T- helpper cells. The T- helpper
38:02cells will help the blymphosy help the
38:04bymphosy do what? Grow up and class
38:08switch. Class switch from what? from IGM
38:11and IGD to everything including IGG, IG
38:15A, IG. So when the site was very
38:19naive, it only had IgM and IG D, just
38:23the M and the D. The way I remember this
38:26is to think of the BMOite in the
38:29beginning as a naive doctor MD. later
38:33when it grows up and matures and class
38:36switches it switches the types or the
38:40classes of antibodies from IGM and IGD
38:43to everything you can imagine including
38:46IGG IG and IG that's why I've told you
38:50earlier in this video that IGM is
38:53responsible for the primary response
38:56whereas IGG is for the secondary
38:58response after you mature after you
39:01class switch after you recognize the
39:04antigen because this conjugated vaccine
39:08activated the T- cells and the T- cells
39:10activated the B cells and the B cells
39:12class switched and the B cells are going
39:15to make memory cells. This vaccine
39:17usually does not require a booster.
39:21That's how strong it is. That's how
39:23important your T lymphocytes are.
39:26Moreover, the Tymphosytes also help kill
39:29cancer cells. So take good care of your
39:32tale lymphosytes. Here is an
39:34illustration of the bumpymphocyite class
39:37switching from the naive doctor MD only
39:40IGM and IGD to a brilliant experienced
39:45seasoned doctor that can make everything
39:48you want including IGG, Ig and Ig. To
39:51learn more about the mechanics of the
39:53class switching, please refer to my
39:55video titled B cell activation and class
39:58switching in this immunology playlist.
40:01And here is how the waiter, the antigen
40:04presenting cell, activates the customer,
40:06the Tymphosite, by presenting the
40:09antigen on a tray of MHC. To learn more
40:13about this process, watch my video
40:15titled T-C cell activation. How do these
40:18cells talk to each other? The answer is
40:20by means of cytoines. What are cytoines?
40:24First let me tell you what the word
40:25means. Cyto means cell kind from kinetic
40:29to move. Oh so these are a bunch of
40:32chemicals or particles that help your
40:35cells move i.e do something cause an
40:38action to happen. Cytoines are many and
40:41we divide them into many groups such as
40:43interlucans colony stimulating factors
40:46and tumor necrosis factors. I've talked
40:49about these guys in my pathology
40:50playlist. Pay close attention to my
40:53video on interlucans which was epic with
40:56tons of pneumonics to help you remember
40:58them. Do you remember the tray? Oh, the
41:01tray is the MHC. The MHC has many types.
41:04I've talked about them in great detail
41:06in a video titled MHC which you can find
41:10in my rheumatology playlist. Remember
41:12that the bumpy and the tymphosytes are
41:15made in the bone marrow. They grow up in
41:17the bone marrow for the B and thymus for
41:21the T and then they work in the lymph
41:24node and in the spleen. I've talked
41:27about lymph nodes in their own video in
41:29my anatomy playlist. You can find my
41:32video on the spleen also in my anatomy
41:35playlist. Fun facts. Is the fetus
41:38genetically identical to the mother? The
41:41answer is no. Is the fetus
41:43imunologically identical to the mother?
41:45If the answer is no, then how come the
41:48mother's immune system does not attack
41:51the baby? For two reasons. Number one,
41:54pregnancy induces a state of immuno
41:57deficiency in the mother, meaning the
41:59mother makes fewer antibodies etc. Which
42:02means the mother becomes less likely to
42:05attack the fetus. Moreover, there is a
42:08barrier called the placenta. It's a
42:10barrier between the mother and the
42:12fetus. This is very similar to the blood
42:14testus barrier. Think about it. How many
42:18chromosomes are in the sperm? The answer
42:20is 23. How many chromosomes are in the
42:23rest of the male body? The answer is 46
42:26chromosome in every cell of the human
42:28male except for the sperms. Then how
42:31come the immune system does not attack
42:34the foreign sperm which looks very
42:36different from the rest of the body? The
42:38answer is because your cerolei cell made
42:42a blood testice barrier to protect the
42:46sperm from being recognized by your
42:48immune system. Destroy that blood
42:51testice barrier and now you're toast.
42:55Destroy that blood placental barrier and
42:58the fetus is toast. Since the mother is
43:00imunosuppressed during pregnancy, we
43:02will not give the mother live attenuated
43:06vaccine during pregnancy because the
43:08mother's immune system can't handle the
43:11truth. I mean the vaccine. Can you give
43:13me examples of live attenuated vaccines?
43:16Certainly. Measles, ms, reubella, polio
43:19influenza, vicella and yellow fever. Do
43:22not give these during pregnancy. careful
43:25because there are many different types
43:27of the influenza vaccine and many types
43:29of the polio vaccine. Now, my immune
43:32system is very good at attacking foreign
43:34invaders. But how come the immune system
43:36does not attack me? Well, your immune
43:39system does not attack you because your
43:41immune cells can recognize the self and
43:45become tolerant to the self, i.e. does
43:48not attack your cells. Your immune
43:51system is capable of distinguishing
43:53between the self I'm not going to attack
43:56this versus the non-self. I will destroy
43:59this. And that's why you have the
44:01T-uppressor cells. Now we call it T-
44:03regulatory cells, but I love the old
44:06name better. T-uppressor. Why? Because
44:08it suppresses the ability of your immune
44:11system to attack your own cells. It
44:15suppresses the attack against the self.
44:18Destroy your tea suppressors and you
44:21will be destroyed by your own immune
44:24system. Welcome to the land of
44:26autoimmune diseases. These are a bunch
44:28of diseases in which your immune system
44:30attack you. What a load of rubbish.
44:34Example of autoimmune disease include
44:36type 1 diabetes where you have nasty
44:38antibodies against the beta cells of
44:40your pancreas, myastthenia gravis in
44:43which you have nasty antibodies against
44:46the nicotinic subm receptor otherwise
44:48known as the acetylcholine receptor on
44:51your own skeletal muscles. Celiac
44:54disease where you have nasty antibodies
44:56attacking tissue transglutamines
44:58in your small intestine as well as
45:01rheumatoid arthritis attacking your
45:03joints and systemic lupus aromthitosis
45:06attacking your joints and your heart and
45:09your lungs and your mucous membrane and
45:12your bone marrow and your kidneys and
45:14every organ you can imagine. And that's
45:16why Dr. House always says it's lupus.
45:20It's always lupus. When in doubt, say
45:23lupus. When in doubt, give
45:26corticosteroids. That's practically how
45:28most doctors today roll. It's always
45:31corticosteroids because when doctors
45:34don't know what to do, they give
45:36steroids to you. And they usually work.
45:39And that's why I call steroids the
45:42stupid doctor's savior. Now we'll talk
45:44about the compliment system which was
45:47discussed in its own video in my
45:50physiology playlist and in my immunology
45:52playlist. Why do we call it compliment?
45:55Because it complements the ability of
45:58your antibodies and fagocitic cells to
46:00perform their function and to do their
46:02job. I.e. it complements your immune
46:05system. Is the complement system active?
46:08Of course. Of course it's going to do
46:10stuff. Listen to me carefully. Anything
46:12that's active in your body is mostly a
46:14protein. Think of all of the
46:16macroenzymes you study in biochemistry.
46:19Most, if not all of them are proteins.
46:21How about the receptors? They're
46:22proteins. How about the pumps? Proteins.
46:25The carriers proteins. The channels
46:28proteins. The cell adhesion molecules
46:30proteins. And the complement is made of
46:33a bunch of proteins. We're going to call
46:36them C, such as C1, C2, C3, etc. C
46:41stands for compliment. Let's talk about
46:43the structure of the compliment system,
46:44the function, the pathways because we
46:46have three separate pathways. The
46:48biological effects of the compliment,
46:50how to regulate it, and what happens
46:52when the compliment is not well
46:54regulated. What happens when your
46:56compliment malfunctions? It's not good.
46:59The compliment system, a bunch of
47:01proteins such as C1, C2, C3, all the way
47:04until C9. It's a family of proteins
47:08acting together in harmony. who makes
47:10them. Like most proteins, they're made
47:12in the liver. Most of the biochemistry
47:15textbook takes place in your liver. Take
47:17good care of your kidneys, but if you
47:19don't, we have dialysis for your
47:21kidneys. Take good care of your liver,
47:24but if you don't, there is no dialysis
47:26for your liver. Without your liver,
47:28you're toast. You'll be lucky if you
47:31have an organ transplant donor
47:33available. But in most cases, you won't.
47:35So, take good care of your liver. Do not
47:37drink, especially excessively. Do not
47:40take acetaminophen or tylenol or
47:42paracetamol especially excessively. Do
47:45not become morbidly obese because this
47:47can lead to fatty liver disease. Avoid
47:49hepatitis A, hepatitis B, hepatitis C,
47:52hepatitis D, and hepatitis E. Avoid the
47:54liver fluke and any other fluke. What's
47:57the technical scientific name of the
47:59liver fluke? If you know, comment below.
48:02Is the compliment system part of the
48:04innate immunity or the adaptive
48:06immunity? The answer is it's kind of
48:08both. It's actually the bridge that
48:10bridges the gap between the innate
48:12immune system and the adaptive immune
48:14system. The compliment system acts like
48:17a cascade, like a waterfall. What else
48:20was a cascade in the human body? If you
48:23say the coagulation cascade, you're
48:25absolutely correct. See my bleeding and
48:27coagulation playlist. Why is the
48:30compliment a cascade? Why is the
48:32coagulation or the secondary hemostasis
48:35a cascade? The answer is because every
48:38step is stronger than the previous step.
48:41You keep getting stronger and stronger
48:43and stronger and stronger and stronger
48:45and then bam, you destroy the bacteria
48:47or bam, you coagulate your blood to
48:50prevent bleeding. Moreover, if you have
48:52multiple steps rather than one singular
48:55explosion, it will be easier to regulate
48:58said steps. In the coagulation cascade,
49:02the fibbrinogen became fibbrin.
49:04Fibbrronogen is not active. Fibbrin is
49:07active. Fibbrinogen is a very big
49:10molecule. Fibbrin is a little smaller.
49:13How do you activate fibbrroen to
49:15fibbrin? By breaking down the big
49:19fibbrinogen into the smaller fibbrin,
49:22you activate by destruction. What the
49:25economist Joseph A. Chumpeter might call
49:28creative destruction. You activate by
49:32cleavage, by breaking down the bigger
49:35protein into the smaller protein. It's
49:37proteolyis. It's a cleavage. No, not
49:40that kind of cleavage that you're
49:42thinking of, you dirty lad. So you
49:45activate by breaking down. Who broke
49:48down fibbrinogen into fibbrin? The
49:50answer is proth thromben which means
49:52that proth thrombin has proteolytic
49:55activity to break down proteins. By the
49:58same token the compliment proteins start
50:01as big and inactive. You can call them
50:04inactive or pro-enzymes or zyogens.
50:07Through creative destruction i.e.
50:09cleavage meaning proteis you activate
50:13them and when the complement protein is
50:15active you put a hyphen or a dash or a
50:18bar on top. So C1 is not active C1 bar
50:22is an active C1 compliment protein. He
50:27who has a Y to live said N can bear
50:30almost any how. He who has a Y to the
50:33compliment said Moses can bear almost
50:36any cascade. Why? Why do I need
50:39compliment? You need compliment for
50:41aglutination, for bacterial opsinization
50:43to make them tasty so that you can kill
50:46them better. For chemotaxis to attract
50:49your neutrfils from the inside of the
50:52vessel to the outside, you cause them to
50:55move taxi by means of chemicals. Chemo
50:59put it together chemotaxis for direct
51:02cell killing. The compliment will help
51:04you neutralize i.e. to render powerless
51:07the toxins of viruses to change them
51:10from virilent to nonvirolent or less
51:13virulent. Also, the compliment can
51:15complement the ability of your mass
51:18cells and the basoils to make histamine.
51:20He who has a Y to the compliment can
51:23bear almost any cascade. This is why we
51:26do it. We do it to destroy invaders. So,
51:29the compliment system has one main
51:32function which is to kill foreign
51:34invaders. How do you kill it? By a
51:37weapon. What's your weapon? Major attack
51:40complex or MAC. And the MAC will attack
51:44the bacteria. The MAC is also known as
51:46TCC or terminal complement complex
51:49because it comes at the end terminal. So
51:52the end result is the same. You're going
51:54to destroy the invader. However, who
51:58pulls the trigger? Well, I have three
52:00different people that can pull the
52:02trigger. I.e. three separate cascades.
52:05The end result of all of them is to make
52:08the MAC and the MAC will attack the
52:10bacteria. Who pulls the trigger? In the
52:13classical pathway, the antigen antibbody
52:15complex pulled the trigger. In the
52:17alternative pathway, the bacterial
52:20endotoxins and properin pull the
52:22trigger. In the lectin pathway, it's the
52:25manos binding lectin or the manan
52:27binding lectin that pulled the trigger.
52:30Whether you pull the trigger by the
52:32antigen antibbody complex or the
52:34bacteria intoxins or the man who is
52:35binding lectin, the end result is the
52:37same. You're going to form a MAC and the
52:40MAC will attack the bacteria. Since the
52:43MAC came later rather than earlier, we
52:46call it the late complement or the
52:49terminal complement complex TCC. What is
52:52the MAC? The MAC is made of C5B, C6, C7,
52:56C8 and C9. If you are lazy, just say C6
53:00through C9. The end is the K9 which will
53:04attack the criminal if you happen to
53:06watch Law and Order. So the end is the
53:09K9. Do not just keep continuing C10 and
53:11C11 and C12. Just stop at the K9. Before
53:15I had C5B, I had C3B. Keep this in mind.
53:20C3B has two main functions. Number one,
53:22it helps us form the Mac and the MAC
53:25will attack. Function number two, it
53:27helps opsinize i.e. to render tasty the
53:31foreign invader that you're trying to
53:33destroy. Please note that in the
53:36alternative compliment pathway, the
53:38trigger is pulled by the bacterial
53:40endotoxin. And in the lectin pathway, we
53:42pull the trigger by the manos. When
53:45bacteria invade your body, do they come
53:47with their toxins? The answer is yes. So
53:49this does not require secondary
53:50exposure. You can find this from the
53:52first exposure. before you even form an
53:55antigen antibbody complex. Okay, how
53:57about the lectin pathway? Yep, it comes
53:59with the manos baby which means that's
54:01my first exposure. This is innate.
54:04However, later when you form an antigen
54:06antibbody complex even then you can
54:09still activate the compliment by means
54:12of the classical pathway and this is the
54:14secondary exposure. This is adaptive and
54:17that's why I've told you before and I
54:19will tell you again that the complement
54:22bridges the gap between the innate
54:25immunity and the adaptive immunity. Once
54:28you have C3B, what's the next step? It's
54:30called C5 convertase. Keep this in mind.
54:33The C5 convertase will convert C5 into
54:39C5A which will go away A away and C5B
54:45which will continue to be part and
54:47parcel of the complement cascade until
54:50you for the MAC and the MAC will attack.
54:52By the same token, the C3 complement
54:55protein by an enzyme known as C3
54:58convertase which will convert C3 into
55:02C3A and C3B. What's going to happen to
55:05C3A? It will walk away with the A. But
55:09C3B will continue to be part of the
55:12complement system. After C3, there is
55:15C5. By C5 convertase you will convert
55:19the C5 complement protein into C5A which
55:23will walk away and C5B which will
55:27continue to be part of the compliment
55:29cascade until you form the MAC and the
55:31MAC will attack. So C3 by C3 convertase
55:36will give us C3A and C3B. C3A will walk
55:39away. C3b will continue to be part of
55:42the complement. Then you form a C5
55:44convertase which will convert C5 into
55:48C5A and C5B. C5B will continue to be
55:52part of the complement until you form
55:54the MAC and the MAC will attack. The A
55:56fragment whether C3A or C5A is always
56:00leaving the cascade whereas the B
56:02fragment be it C3B or C5B stays in the
56:06cascade. Why does the C3A and the C5A
56:09walk away? What are they trying to
56:11achieve? Well, they have another
56:12function. If it ends in an A, it's an
56:15anletoxin, i.e. it causes anaphylaxis.
56:19And anaphylaxis is a type one hyper
56:22sensitivity reaction. It's part of your
56:24immune response. Whereas the B fragments
56:27C3B, C5B will continue to be continue to
56:31bide within the compliment and bulldoze
56:34the cascade forwards. Let's put all the
56:37three compliment pathways together.
56:39Here's the classical pathway. Who pulled
56:41the trigger? Antigen antibbody complex.
56:44Here's the alternative pathway. Who
56:46pulled the trigger? Lipopolyaccharides
56:49of the bacteria, parts of the fungus,
56:51parts of the virus. And don't forget
56:53proper. Third, in that lectin pathway,
56:56you have mann binding lectin which
56:58pulled the trigger. Whether you pull the
57:00trigger here, here, or here, the end
57:02result is the same. It's the C3
57:04convertase which will convert C3 into
57:08C3A and C3B. C3A walks away just like
57:12C4A, C2A and C5A. C3B continues to be
57:16part of the compliment. C3B among others
57:19will form C5 convertase which will
57:22convert C5 into C5A walk away and C5B
57:27continue to be part of the MAC. The MAC
57:30will attack. C3B has another function
57:32which is optinization. gather all the
57:35A's together, the C2A, C4 A, C3A and C5A
57:39and they have another function
57:41anletoxins. C3 convertase could be this
57:45guy or that guy depending on the
57:47pathway. In the classical and the lectin
57:49pathway, C3 convertase is a complex of a
57:52bunch of proteins. They are C4B and 2B.
57:56But in the alternative complement
57:58pathway, the C3 convertase is made by
58:00C3B and BB. How about the C5 convertase?
58:04You simply take what you just said and
58:06add 3B to that. So the C5 convertase is
58:10made of C4B 2B 3B if you are in the
58:14classical or the lectin pathway. The
58:16same C5 convertase is made of C3B BB 3B.
58:21If you are part of the alternative
58:23pathway, keep in mind the following. If
58:25you are reading from an old textbook or
58:28from your professor's PowerPoint which
58:30has never been updated, you might see
58:33that 2B is written as 2A. This is the
58:37old name. It was called C2A in the past.
58:40Now we call it C2B. So it's the same
58:42thing. It's still the same protein. So
58:45whether you want to call it C4 B to A or
58:48C4 B to B, it's referring to the same
58:51exact thing. So what was called C2A in
58:55old textbooks is now called C2B in
58:59modern textbooks. Now let's talk about
59:02regulation of the compliment. Next
59:04regulation of the complement. If you see
59:06that green color, it means that this
59:08thing is going to activate the
59:10compliment. If you see a red color, it
59:12means that they will inhibit the
59:14compliment. So antigen antibbody
59:16complex, of course, they activate the
59:17classical pathway. They activate the
59:19compliment. C1 strace inhibitor inhibits
59:22the compliment. Factor H inhibits the
59:24complement. It becomes factor I. I for
59:27inhibition inhibits the complement.
59:29Propertin or factor P stimulates and
59:33propels it forwards. Decay accelerating
59:35factor. It's death and decay. It
59:37inhibits the compliment. This is part of
59:39the classical pathway. Classical
59:41pathway. Alternative and alternative.
59:43You need to know something about the
59:45decay accelerating factor. It inhibits
59:47the compliment. It inhibits the C3
59:49convertase and the C5 convertase. Why do
59:52you want to inhibit the compliment? Why
59:54is this part of your natural system? The
59:56answer is because I do not want the
59:59compliment to attack my own cells. Oh,
1:00:02now what if you are missing the decay
1:00:05accelerating factor? This is like
1:00:07driving without the brakes in your car.
1:00:10If you cannot stop the compliment from
1:00:12attacking your cells, you will attack
1:00:16your cells such as your red blood cells.
1:00:19Now your red blood cells are toast. They
1:00:21will destroy themselves. You will get
1:00:23hemolysis. This is seen in a disease
1:00:26known as parogismal nocturnal hemoglobin
1:00:30ora where you have hemoglobin in the
1:00:32urine because you kept breaking down
1:00:35your red blood cells because you're
1:00:37missing the decay accelerating factor.
1:00:40I've talked about peroxismal nocturnal
1:00:43hemoglobinura in its own video in my
1:00:45hematology playlist. Now what happens in
1:00:49diseases? Well, whether you are not
1:00:51making enough compliment proteins or
1:00:54you're consuming them too quickly,
1:00:56either way, you can get sick. Welcome to
1:00:59the land of pathology. The clinical
1:01:01implications or the diseases related to
1:01:04the compliment system were discussed in
1:01:06detail in my video titled the compliment
1:01:09system which you can find in this
1:01:11immunology playlist. And one more thing,
1:01:15hypers sensitivity reaction. hyper
1:01:17sensitivity or when your immune system
1:01:21overreacts. Hypers sensitivity reactions
1:01:24are immune mediated inflammatory
1:01:27diseases. I've talked about them in
1:01:29great detail in a separate video in my
1:01:32physiology and pathology playlists.
1:01:35There are four different types of
1:01:36hypersensitivity. Type one, type two,
1:01:39type three, and type four. Some stupid
1:01:42books divide them into five types.
1:01:45That's a mistake. If your professor told
1:01:48you that there are five types of hypers
1:01:50sensitivity reactions, well, what your
1:01:53professor called type five is nothing
1:01:56more and nothing less than a weird
1:01:59subtype of type two. Hypers sensitivity
1:02:02reactions include type one, type two,
1:02:04type three, and type four. Type one is
1:02:07the fastest, i.e. the quickest, the most
1:02:09immediate, but type four is so slow.
1:02:13It's the delayed type hypers sensitivity
1:02:16reaction. As you go from type one toward
1:02:19type four, it's getting slower and
1:02:22slower and slower. So, type one takes
1:02:24seconds to occur. Type four takes two to
1:02:28three days to take place. Two and three
1:02:31are in between. Type one
1:02:33hypersensitivity is also known as
1:02:35immediate type hypersensitivity or the
1:02:38anaphylactic type of hypersensitivity.
1:02:40Say hi to your Ig, to your masked cells,
1:02:44to the histamine, and to the
1:02:45eosinaphils. What did I tell you about
1:02:47Ig and about the einaphils? It's ew.
1:02:51Allergies, ew. Anaphilaxis, ew.
1:02:54Parasites, double triple E. Type two is
1:02:58cytotoxic. What does cyto mean? It means
1:03:01cell. Okay. Why do you call it
1:03:03cytotoxic? Because we have an antigen
1:03:06and antibbody reacting on the surface of
1:03:09the cell cyto this antigen is insoluble
1:03:13meaning it's not soluble in the blood
1:03:15it's not floating in the blood but
1:03:17rather fixed to the cell surface that's
1:03:20type two s2 toxic but type three is free
1:03:24you have antigen antibbody complexes or
1:03:26immune complexes freely floating in the
1:03:29blood i soluble that's type three very
1:03:33free and type four is the most delayed.
1:03:36It's the slowest one. Unlike the
1:03:38previous three types of
1:03:40hypersensitivity, type four uses no
1:03:42antibodies whatsoever. I don't care
1:03:44about Ig or IgM or IGG. Unlike the
1:03:48previous types, type 4 does not care
1:03:51about baleymphocytes because remember it
1:03:53was the bale lymphocytes that became
1:03:55plasma cells and gave us the antibodies
1:03:58whether IG or IGM or IGG but rather the
1:04:02type 4 hypers sensitivity reaction is
1:04:05pecularly
1:04:07tlymphosetic
1:04:08in nature and of course that these cells
1:04:11talk to each other by means of cytoines
1:04:13such as interlucan one interlucan 2 etc.
1:04:17Type one takes seconds to minutes. It's
1:04:20the immediate type of hypersensitivity
1:04:22reaction. Does it have antibodies? Yes,
1:04:24it has Ig. So, it's hemoral. It's B
1:04:27lymphocytes, not Tlymphosytes. This is
1:04:30the land of mass cells and basopils and
1:04:33histamine and Ig and anaphilaxis with an
1:04:36A. Attopi with an A, including attopic
1:04:40dermatitis, asthma with an A, bronchial
1:04:43asthma, allergic rhinitis with an A, hey
1:04:47fever with an A. Hey fever, how are you?
1:04:50What's up? Allergic conjunctivitis,
1:04:53allergy to food, allergy to medications.
1:04:56And finally, B, the bee sting. If a bee
1:05:00stings you or a bunch of bees sting you,
1:05:02this can be fatal because it's type one
1:05:05hyper sensitivity. Within minutes,
1:05:07you're toast. You need to go to the
1:05:09hospital very quickly. And before you go
1:05:12to the hospital, the EMS people of the
1:05:15ambulance should give you epinephrine or
1:05:18adrenaline. Because when you are in a
1:05:20state of anaphylactic shock, you have
1:05:22very low blood pressure. Epinephrine
1:05:25will raise your blood pressure. When you
1:05:28are in a state of anaphilaxis, your
1:05:30bronchi are very constricted and you're
1:05:32winging. You cannot breathe. But
1:05:35epinephrine tends to dilate your
1:05:37bronchi. How about type two hyper
1:05:39sensitivity action? It's s2to toxic. We
1:05:43have an insoluble antigen bound to the
1:05:45surface of the cell. An antibbody will
1:05:47recognize that antigen. In most cases
1:05:50you will destroy that cell as in
1:05:53myastthenia gravis, pimpus vulgaris,
1:05:55rheumatic fever, good pasture syndrome
1:05:58etc etc etc. In only one situation
1:06:02that's the weird one. You're going to
1:06:04stimulate the target cell and this is
1:06:06Graves disease where you have nasty
1:06:09antibodies stimulating. Yes, you heard
1:06:12that right. Stimulating the target. The
1:06:15thyroid gland is being stimulated by
1:06:17antibodies. That is very weird and
1:06:20that's why your professor might call
1:06:22this particular type five hypers
1:06:25sensitivity reaction. I have no idea
1:06:28where professors get type five from
1:06:30because most respected textbooks whether
1:06:34of immunology, pathology, physiology,
1:06:36internal medicine, you name it. All of
1:06:39them recognize hypersensitivity
1:06:41reactions as four types only. But now
1:06:44you know what the professor means. How
1:06:46about in type three? Type three is free.
1:06:49The antigen is free meaning soluble.
1:06:51Soluble in the blood. We have antigen
1:06:53antibbody complex in the blood. This
1:06:56antigen antibbody complex or immune
1:06:58complexes can destroy the wall of your
1:07:01blood vessel. This is called immune
1:07:03mediated vasculitis. They can flow and
1:07:06flow and flow until they hit your
1:07:07kidneys. Immune mediated nefritis. Or
1:07:11they can destroy your joints. Immune
1:07:13complex mediated arthritis. immune
1:07:16mediated vasculitis, immune mediated
1:07:18arthritis and immune mediated nefritis.
1:07:22It's like tell me you have lupus without
1:07:25actually telling me. Type four hypers
1:07:27sensitivity is the delayed. It's cell
1:07:30mediated by the tymphosytes. No
1:07:32blymphosytes and no antibodies unlike
1:07:34the rest of the sheep. Tlymphosytes with
1:07:37the help of macrofasages can make
1:07:39granulomaas.
1:07:40You see granulomaas in tuberculosis. We
1:07:44see granulomaas in syphilis in leprosy.
1:07:47What's the name of the granuloma of
1:07:48tuberculosis? Tuberculoma. What's the
1:07:51name of the granuloma of leprosy?
1:07:53Lepoma. And what's the name of the
1:07:55granuloma of syphilis? It's called gma.
1:07:58Gu m a. Who else is going to teach you
1:08:01like this? Your professor with his
1:08:03powerpoint. Give me a break. Some
1:08:05granulomaas are caseiating as in
1:08:07tuberculosis, hystopplasmosis,
1:08:09blastoicosis, and coxidoid micosis.
1:08:12Almost every other granuloma is
1:08:14non-asiating including sarcoidosis
1:08:16non-asiating Crohn's disease
1:08:19non-casiating
1:08:20foreign body granuloma non-asiating etc
1:08:24meaning if I inject a foreign body under
1:08:27your skin you will react to that foreign
1:08:30body but it takes two to three days it's
1:08:32a delayed type four hyper sensitivity
1:08:35reaction who sustains the granuloma just
1:08:39like food sustaining humans the Answer
1:08:41is interferon gamma. To learn about type
1:08:441 hypers sensitivity reaction with its
1:08:46interlucan 4, interlucan 5, Ig,
1:08:50eocinophils, histamine, serotonin and
1:08:52eocinophilic chemotactic factors. And to
1:08:55learn about type 2 hypersensitivity
1:08:57reactions, whether compliment mediated
1:08:59or non-complent mediated to learn about
1:09:02the generalized and the localized
1:09:04subtypes of type three hypersensitivity
1:09:07reaction. and as well as type four hyper
1:09:10sensitivity reaction that we see in the
1:09:12tuberculosis skin test. Go watch all my
1:09:15videos on hypersensitivity in my
1:09:17pathology playlist. They shall immunize
1:09:20you against ignorance and naivity. No
1:09:24pun intended. These are all the topics
1:09:26that we talked about today. Remember
1:09:28that your blood is made of plasma and
1:09:31blood cells. Your plasma is made of
1:09:33water, electrolytes, and plasma
1:09:35proteins. Your blood cells are red blood
1:09:37cells, white blood cells and platelets.
1:09:40The white blood cells are part of your
1:09:42immune system. You have innate immunity
1:09:44and adaptive immunity. Humoral immunity
1:09:46by the B cells and cell mediated
1:09:49immunity by the T- cells. The complement
1:09:51system complements the function of the
1:09:54antibodies and of the fagocitic cells.
1:09:57The hypers sensitivity reactions are
1:10:00nothing more and nothing less than
1:10:02immune mediated inflammatory diseases
1:10:05and they come in four flavors. Hopefully
1:10:09you learned something today. If you want
1:10:11one PDF file that summarizes all of the
1:10:15leukemias for you, go to my website
1:10:17medicosperfictionalis.com
1:10:19and download my pun leukemia. I also
1:10:22have a perfectionalis ultimate notebook
1:10:24on lymphas. These come with lots of
1:10:27notes and lots of cases. If you value
1:10:30what I do, help me make more videos by
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1:10:55personally tutor you. Be safe, stay
1:10:57happy, study hard.

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