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USC BISC 307L - Mechanisms of Acquired Immunity II
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Major Histocompatibility ComplexAll cells produce at least one of the MHC moleculesEach nucleated cell is labeled with a large complement of unique moleculesNon nucleated cells don’t have MHC molecules ( red blood cells) Only have 2 glycosurface proteins used for recognition called A and B. Those that don’t have either are OClasses of MHC ProteinsClass 1Expressed in all cells with nucleiPresent antigens to T cellsCytotoxic T cells and helper T cells will recognize antigens by the antigens binding to the T cell receptorsHas a lot of variability in the antigen binding siteAlpha and beta chainsT cell receptor binds to the antigen but T cell receptors don’t bind to naked antigens like B cells. The T cell receptor must also bind to the MHC class I presenting the antigen and must be stabilized by CD82 T cell receptors binding to two things presenting the antigenAntigen is presented by MHC class 1 (like a sample of peptides being made inside the cell)This is a strong binding and if a helper T cell agrees then it will activate the cytotoxic T cell and the cell will be killed by apoptosisClass II MHC proteinExpressed on the surface of dendritic cells , macrophages, and B cellsClass II MHC also pick up samples of peptides in the cell that are part of the endocytotic processPhagocyte displays to lyphocytes a sample of antigens from things that have been phagocytizedThe helper T lyphocyte is receiving the signalThis T cell receptor binds antigen and class II MHC receptorHas CD4 to stabilize the bondingInterleuken I cytokine helps stimulate the helper T cellHelper T cells mostly stay in the lymphoid tissues and the MHC cell comes to themActivation of B lymphocytesThis on left is macrophage presenting fragment of antigen to class II MHC molecule and this activates the helper T cell. Weak activationnot fully activated unless B cell agreesTriggers phagocytosis by the B cell the B cell presents those antigens to a helper T cellMust be activated by phagocyte and B cell3 cells agreeing that something needs to be doneresults in active B lymphocyte and helper T cellThe helper T cell when activated is secreting cytokines to activate the B cellThe b Cell when fully activated will proliferate to form plasma cells and memory cellsAntibodies secreted IgMIgGAntibodies secreted at a rate of 2000/secondThere is a delay upon first exposure to antigenthen there is a rise that lasts for several weeksThe large clone of memory B cells and memory helper T cells will persist and may live for the rest of your life and upon second exposure to the antigen are capable of a faster immune response (Basis for vaccination)Probably don’t even know you got sick the second timeActivation of Cytotoxic T lymphocytesActivation of Cytotoxic T cells. Active during responses to viral infection and cancerVirus infected cell is displaying on its surface via class MHC I bearing antigenThis will activate Cytotoxic T cell but it is weak so needs agreement from helper T cell that there is a viral infection that needs to be attacked.Activated helper T cell secretes interleukin 2 and this is needed for the cytotoxic T cell to be fully activatedproliferate into clonal and memory cells. Clonal cells will kill the cell from withinThe active cytotoxic t cell moves on and looks for more infected cellsChemical Communication Between Macrophages and T lymphocytesCytokines are hormones (endocrine and paracrine)This reemphasizes the chemical communicationThe chemical communication is due to interleukin 1 acting as a paracrine hormoneThe helper T cell secretes interleukin 2 and causes macrophage to secrete tumor necrosis factor and causes prevention of cancerCytotoxic t cells bring about their own destruction by once they are activated they start to express protein called FAS receptor. These don’t do anything until later when they express FAS ligand and this triggers apoptosisEliminates potential dangerThis is exploited in compartments of the body that are immunologically privileged sites- certain parts where cytotoxic T cells are not allowed (Testes- developing sperm cells secrete protein that would cause apoptosis by cytotoxic T cells. But sertoli cells secrete an FAS ligand and keep cytotoxic T cells out of the Testes) Also (anterior chamber of the eye. Site where cytotoxic T cells aren’t allowed. Prevents clouding of the eye. The epithelial cells that line this area also express FAS ligand and express molecules that suppress inflammationOne of the characteristics of some types of cancer is the expression of FAS ligand on the surface. Will protect itself from cytotoxic killingImmunological ToleranceWhy don’t we die of autoimmune attack?Old idea: during embryonic development T and B lymphocytes acquired receptors at random and could respond to anything that might be out there. *old view says that at some point late in fetal life, T and B cells are tested by presenting antigens to them (mostly class I) and any T or B cell that responds to self antigens triggers apoptosis. So left with T and B cells that don’t respond to self cellsNew idea: found this isn’t true. Would expect to find T and B cells that don’t respond to self antigens. Found that actually most respond to self antigens. Current view: late in fetal development the cells are tested in bone marrow and thymus and there are 3 possibilities1. Response will be strongvigorous response is killed by apoptosis (clonal deletion)2. Weak responseAlso killed by apoptosisMakes sense because all kinds of mutations are allowed to accumulate and high rate of defective cell. Any cell that isn’t capable of responding is seen as defective3. Moderate responseProven that functionalBut only responding moderately they’ve proven that they are not that dangerous and can be controlledThis is called positive selection- these are the ones that stay1. How do you test for reactions to cells that aren’t in the thymus and bone marrow?During this testing period, the bone marrow expresses tissue from other organs (liver or kidney)2. New T and B lymphocytes are actually produced throughout life and go through this screening not only in fetal life. Do not stop at the end of fetal lifeexample: during pregnancy new huge thing growing inside of her and half of the genome is foreign. Why isn’t the fetus killed?The mother’s immune system is adapting and tolerates itAnother example: organ transplants. Never will have a perfect match. There is always an immune response so there are


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USC BISC 307L - Mechanisms of Acquired Immunity II

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