what's going on everybody it's medicosis perfectionist where medicine makes perfect sense let's continue our physiology playlist in the last video we talked about the hemoral immunity or the b cell immunity today it's time to talk about the cell mediated or cellular immunity or t cell immunity b lymphocytes mainly defend your body against bacteria but t lymphocytes defend your body against viruses and fungi Joe Rogan may relate. Now let's get started. Who secretes antibodies? Plasma cells. Where do they come from? From B lymphocytes. What happens when your antibody meets the foreign antigen? neutralization of the bad antigen, opsonization, make it tasty, agglutination, activation of the natural killer cell to kill those bacteria, and activation of the complement system. Remember, the antigen antibody complex activates the classical pathway of the complement. We have three complement pathways. Number one, the classical pathway. Number two, alternative pathway. Number three, Manose binding lectin pathway. How do your immune cells, such as the lymphocytes, communicate with each other? They release cytokines. What does cyto mean? Cell, because they are talking to each other, and they are cells. Kines from kinetic motion. Oh, some secreting chemicals to put these cells in motion. Love it. Here's the most basic idea of cytokines. They are divided into... Three categories. The interleukins, colony stimulating factors, and tumor necrosis factor. IL, CSF, TNF. What does inter mean? Between leukocytes or white blood cells. IN is a protein or peptide or whatever. So interleukin literally means the internet of the leukocytes. I love it. This is how they communicate with each other. Colony stimulating factors. Factors that stimulate the colony. of the white blood cells, for example. And if you remember my previous videos, we talked about G-CSF and GM-CSF, granulocyte colony stimulating factor, and granulocyte monocyte colony stimulating factor. Let's review the story of immunology. Here is a foreign bacteria invading your body. We'll take a piece of it. The piece is called the antigen. And then who's going to present the antigen? Antigen presenting cells. da presented to whom to the lymphocytes and when the lymphocytes recognize the antigen they will stop being so naive and they will grow the French toast up grow to do what to destroy the microbe T lymphocytes especially the T helper cells are going to activate the B lymphocytes so that the B lymphocytes become plasma cells to secrete antibodies or to become memory cells so that we can remember this interaction So that the second exposure to the same antigen is gonna be faster and stronger. We're gonna kick that bacteria in the butt. As you know, the antigen presenting cells could be macrophage, B lymphocytes, or a dendritic cell. B lymphocytes, hemoral immunity. T lymphocytes, cell-mediated immunity. Why do you call this hemoral immunity? Because we're secreting antibodies in the humors, the fluids of the body, such as the serum or your mucous membrane fluid. Why do you call this cell-mediated? Because the cell, by itself, is gonna go and kill this stupid virus face-to-face, cell-to-cell. That's why it is cell-mediated. The T lymphocytes could be T helper, CD4, or T cytotoxic, CD8. The cluster of differentiation is like your identification card. How does the police recognize Adam by his ID? How do you recognize the type of the lymphocytes by their CD? The T cytotoxic is cytotoxic, toxic to cells. I'm toxic to fungi, virus-infected cells, and cancer cells. But T helper is of huge help. I can help my sister. I can help my brother. I can help my neighbor. Okay, tell me about your sister. The T cytotoxic. I am CD4. She's CD8. She's my sister. We're very close. Both of us have CD3 as well. Okay, why would you help the T cytotoxic? To kill foreigners and cancers. How do you help your brother? I help the T regulatory cell, formerly the T suppressor cell, suppress my own immunity a little bit so that I do not attack my own cells, so that I gain tolerance to the self. Otherwise, I will get autoimmune diseases. How do you help your neighbor? I will help my neighbor, the B lymphocyte, to mature and grow the French toast up so that it can become memory cell to remember the same bacteria. When she comes again next time, or to become plasma cells to secrete antibodies into the fluids of my body. Let's activate the T cell. What's that? The antigen-presenting cell. Presenting what? The antigen or the food to the T lymphocyte. And what's the tray on which you put the food? MHC. Okay. If we are activating CD8, we will use MHC class 1. But if we are activating CD4 T lymphocytes... we will use MHC2, so that the product is always 8. MHC class 1 will activate CD8 T-cells, and MHC class 2 will activate CD4 cells. The result is 8. Okay, so now I know that the MHC, major histocompatibility complex, will interact with the T-cell receptor, which is a receptor on the T-lymphocyte. Imagine my shock. But why did we call it major histocompatibility complex? Major because it's a major group of proteins, and there is another group called minor. Complex because it's more than one protein. Histocompatible, I love it. Compatible with my own tissue. And that's why when I saw the bacteria, this was not compatible. Oh, it's about compatibility then. You got it. What's that? This is the ID of the lymphocyte. I could be CD4 or CD8. Whether I'm CD4 or CD8, I'll also have the CD3 ID. This is the first signal. The second signal is CD8086 from the antigen-presenting cell with CD28 from the T-lymphocyte. Everything here is 8. 80, 86, 28. They will interact together. So, here is signal number one, and here is signal number two. That's why we call this signal and co-signal or co-stimulation. CD8086 has another name, B7 protein. Why B7? The way I remember it is that the antigen-presenting cell could be a B lymphocyte, right? Yeah, it's easy to remember. What is acquired immunodeficiency syndrome or AIDS? It's a syndrome which means more than one symptom affecting the same person. Immunodeficiency, my immune system is weak, deficient. Acquired because it's not inherited, it's not congenital, I'm not born with it most of the time. I acquire it later in life. Whether it is through intercourse, parenteral transmission by injections vertical transmission from mommy to baby while passing through the vaginal canal during delivery or from mommy to baby via breastfeeding this is the name of the disease and i've just told you about the route of transmission but what's the cause oh the infectious particle is hiv virus which is an rna virus There are two types of this, or two major types, HIV-1 and HIV-2. Which one is more common? HIV-1. Which one is more global? HIV-1. It's gonna attack my CD4 helper, T-lymphocytes, and therefore, I cannot help my sister, and I cannot help my neighbor. I cannot kill virus-infected cells. and I cannot secrete antibodies. That's why my immunity is frail. Another important point. Mom is different from the baby. Their genetic material is different, and they are immunologically different. And that's why the placenta is so important. The placenta acts as a barrier between the mother and the fetus to prevent the mixing of blood between the maternal and the fetal sides. And in order for mommy not to attack her baby, the pregnancy will induce a state of immunodeficiency, which is protective for the survival of the fetus. That's why we do not give pregnant women live attenuated vaccines, because their immunity is already weak, and live attenuated vaccines contain the live microorganism or the live agent. This could be dangerous during pregnancy. Moreover, the placenta secretes human leukocytic antigen G. Have you ever heard of G? No! I've heard of HLA-A, B, C and HLA-D which is part of MHC-2. I've never heard of HLA-G. Yup, this is unique to pregnancy and G stands for gestation. Do you want your immune system to attack and destroy foreign invaders abso-freakin'-lutely? Do you want your immune system to attack your own cells? Oh, heck no! If my immune system attacks my own cells, I will get an autoimmune disease, which is horrible. Then how come, normally speaking, your immune system does not attack your own cells? How did the immune system tell the difference between the self and the non-self? Gezillion mechanisms. I'll just give you three. Number one, colonel energy. Those T lymphocytes that might get crazy and attack my own cells, we'll just make them weak. We'll weaken them. And no, energy from energy, like no energy. Oh, the T lymphocytes will be stupid and lazy. So that they do not attack my own antigens. How about the one that are super strong against my own cells? Delete them, destroy them, wipe them out. Where did the T lymphocyte mature? In the thymus. Okay, I will destroy it there. also the T regulatory cells formerly T suppressor cells will suppress my own immunity just a little now what if I fail to do all of this your immune system is gonna attack your own cells creating auto antibodies and this is called an autoimmune disease such as type 1 diabetes where you have antibodies attacking your own pancreas especially the beta cells which make insulin myasthenia gravis you have antibodies attacking your own nicotinic sub-M receptor on the skeletal muscle. That's why these patients are weak. We also have celiac disease, which is autoantibodies against tissue, transglutaminase IgA in the small intestine, rheumatoid lupus, and others. There are other topics that you need to know when it comes to the physiology of the blood and the immune system, and this is the ABO incompatibility and the RH incompatibility. They were discussed in great detail in my hematology playlist right here on YouTube. Let's talk about tissue transplant. Okay, here is Adam's kidney, right? Adam is donating a kidney to Sarah because Sarah needs a kidney. As you might have noticed, Adam is different from Sarah. Well, no duh. Adam has a different MHC than Sarah. Yeah, it's major haste to compatibility. Of course, what's compatible with Adam might not be the same as what's compatible with Sarah. Thank you, Captain Obvious. Can this be a problem? Absolutely. Adam gave his kidney to Sarah, but Sarah recognized the kidney as foreign to her and started attacking the kidney and destroying the kidney after the transplant surgery. i don't recognize this kidney this is just some caring behavior right there hey medicosis why are you attacking patients so much why don't you have some respect for yourself yes ma'am i was just joking so how do we prevent this how do we prevent this organ rejection well before surgery we have to do some stuff and after surgery we have to do some stuff Before surgery, match the donor with the recipient. How do I do it? ABO groups, make sure they match. RH groups, make sure that they match. And HLA matching. And then you prepare the patient by suppressing the patient's immunity so that the patient's immune system does not attack the new kidney. And immunosuppressants include glucocorticoids or steroids, cyclosporine, serolimus, tacrolimus. anti-thymocyte globulins, etc. If it is so severe, total lymphoid irradiation. We will destroy serous lymphoid organs so that they do not secrete crazy lymphocytes that attack the new kidney. These medications are not the same. They have different indications, different side effects, etc. And this was discussed in my course called Anti-Cancer Pharmacology, available to download on my website, medicosisperfectsnetis.com. Blood transfusion. Same concept applies. Before you give blood from a donor to a recipient, match them. Make sure they are compatible with each other. Because if they are not compatible, bad things can happen. Antigen antibody reaction destroying the red blood cell. It's gonna rupture. Causing hemolysis and hemolytic anemia. Also, these complexes can clog vessels, causing ischemia and pain. Historically, before we used plastic bags for blood, we used to use glass bottles. The blood will run out and then air bubbles will go from the bottle to the patient's blood, causing air embolism. But now the plastic bags, they will just recoil after the last drop of blood, preventing air embolism. This is huge. If you gave the patient some dirty blood, you might introduce infections. That's why before you give any blood, you need to screen it, make sure that it's healthy and clean and does not contain HIV, hepatitis B, hepatitis C, and others. Back to hemolysis. What are the complications of hemolysis? Remember that this is a red blood cell, right? Red blood cell. So like any cell, it has lots of potassium because potassium is more abundant intracellularly than extracellularly. It has phosphate, remember, ATP, and the membrane has what? Phospholipid, okay, and hemoglobin that's in the red blood cell. So when the red blood cell bursts, it will release tons of potassium and phosphate and hemoglobin into the blood, causing hyperkalemia, hyperphosphatemia. Phosphate and calcium like hate each other. There is an inverse relationship between them. We call this the solubility product. So whenever phosphate goes up, usually... calcium goes down. Hemoglobin. Lots of hemoglobin in the blood is called hemoglobinemia. Eventually, it's going to end up in the kidney. Hemoglobinuria. Hemoglobin can destroy your kidney. Kidney failure and hemocidinuria. Cidero means iron. As you know, hemoglobin is made of heme and globin, and the heme is made of iron and protoporphyrin. These two doofuses are toxic to the kidney. If medicosis has helped you this year, please consider buying me a coffee. Go to buymeacoffee.com slash medicosis. You can get my anti-cancer pharmacology course, my endocrine pharmacology course on my website medicosisperfectsnetics.com and you can get a 40% discount by using promo code KIDNEY at checkout. Thank you for watching. Please subscribe, hit the bell, and click on the join button. You can support me here or here. Go to my website to download my premium courses. Be safe, stay happy, study hard. This is Medicosis Perfectionatus, where medicine makes perfect sense.