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TnTech BIOL 2020 - Cells of the Adaptive Immune System

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Hist 2010 1st Edition Lecture 13Outline of Last LectureCh. 20I. Lymphatic SystemII. Lymphoid Cells and tissueIII. Lymph NodesIV. Other lymphoid organs Ch.21I. Innate Defenses: Surface BarriersII. InternalOutline of Current LectureIV. Cells of the Adaptive Immune SystemV. Humoral Immune ResponseVI. Cellular Immune Response Ch. 21 Part #2- Antigens Typically on the surface of the thing or on the surface of the thing we are talking about  Good: if it is very different than what we have inside of us1. Complete: entire antigens.  Immunogenicity: can stimulate specific clone production Reactivity: able to react with activated lymphocyte2. IncompleteThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute. Haptens- Antigenic Determinants The ability of a molecule to act as an antigen depends on both its size and complexity Immunogenic “plastics” good when hip replacement bad then inhaled at the factory Figure 21.7 pg. 774- Self –Antigens: MHC proteins (bouncers) Dot the external surface of all cells They have a groove in them and they recognize that “self”= MHC Proteins, roam around waiting to find not self then attack it SIV. Cells of the Adaptive Immune System B lymphocytes: oversee humoral immunity, develop in thymus T Lymphocytes: non-antibody-producing lymphocytes, bone marrow develop in bone APCs: do not respond to specific antigens as lymphocytes do. Auxiliary roles. - Lymphocytes Lymphocyte Development, Maturation, and Activation1. Origin: Both B and T lymphocyte precursors originate in red bone marrow2. Maturation: Lymphocyte precursors destined to become T cells migrate to the thymus and mature there, Mat Immunocompetence Self-tolerance 1. : Positive selection:  2. : Negative selection: recognize the MHC and the antigen, making sure T-cells don’t attack body’s own cells3. Seeding secondary lymphoid organs and circulation: recognize self and be ok with self,  Still naïve, exported from the primary lymphoid organs seed the secondary organs,  Generation of Antigen Receptor Diversity Our genes determine which antigens we can resist  Bits and pieces (legos) - Antigen Presenting Cells Going to take something and eat it and then they digest it they take out specific portionsof the membrane and display it as an antigen Dendritic cells Macrophages B lymphocytes Helper T cells activate themV. Humoral Immune Response Activation requires binding of antigen by adjacent receptors Initializes endocytosis and clone formation Plasma cells FORM and SECRETE loads of antibody 2000 molecules/sec For about 4-5 days then they die - Primary Immune Response First exposure to antigen The response has a lag period of 3-6 days Time needed to B-cell proliferation- Secondary Immune response Immune responses are more prolonged, effective, because the immune system has already been primed to the antigen and sensitized memory cells are already “on alert” MEMORY CELLS- Active and Passive Humoral Immunity Active1. Naturally acquired when you get a bacterial or viral infection, could happen with your mother milk2. Artificially acquire when you receive vaccines “prime yourself” Passive Differs by the antibody source and the degree of protection Ready-made antibodies are introduced into your body B-cells are not challenged by antigens  Doesn’t exactly get directly exposed to the virus Baby only last as long as antibodies last only last a few months, stop breast feeding they begin to make their own antibodies  Artificially: We get animals to make antibodies for us, take the disease causing agent inject the horse and get the horse to make antibodies from the injection then bleed the horse. Spin the plasma down and take the antibodies then give the shot of that EX. Tetanus shot - Antibodies Makes up Gamma globulin, B-cellls make gamma globulin Are proteins secreted in response to an antigen by effector B cells called plasma cells and the antibodies bind specifically in that antigen Basic Antibody Structure Going to look like Y shape or T shape  Heavy Chains: Light Chains: half as long as H chains Variable region: the part that is the antigenic binding area, 2 of them on each side identical to each other Constant region: area that are always the same Antibody Classes Ig, MADGE A single B-cell can switch from making one class to the other  Can only make antibodies that only have ultra-specific binding factor, variable region HAS to be the same . binds only the same an Primary immune region igM and igG Secondary immune response igG and IgM: pentamer, snowflake 10 binding sites IgA: dimer, monomer in epithelial surfaces IgD: surfaces of B-cells, B cell antigen receptor IgG: most abundant, readily fixes and activates complement, crosses the placenta confers passive immunity from the mother to the fetus IgE: monomer, stem end binds to mast cells or basophils, releases histamines and other chemicals that mediate inflammation and allergic reactions Antibody Targets and Functions They all have to form antigen-antibody complexes, marks this particular cell or thing is something the body needs to kill1. Neutralization- Simplest occurs when antibodies block specific sites on viruses or bacteria exotoxins. Virus cannot bind to receptors on tissue cells.-2. Agglutination- They can bind to the same determinant on more than one antigen ata time. Results in the cross linking of antigen-antibody complexes- IgM: is a potent agglutinating agent3. Precipitation- Soluble>Insoluble molecules are cross-linked into large complexes that settle out of solution- Precipitated antigen molecules are much easier for phagocytes to capture and eat them4. Complement Fixation and Activation- When several antibodies bind close together on the same cell the complement fixation into the antigenic cells surface followed by lysis.- Encourage inflammation which causes phagocytosis via opsonizationwhich causes a Positive feedback VII. Cellular Immune Response T-cell cell to cell interactions, are naïve if activated the called CD4 and CD8 CD4: surface receptors, become helper T-cells when activated, which activate B-cells, other T-cells, and macrophages and direct the adaptive


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