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Ch. 21 Notes: Immune System Innate Defenses Adaptive Defenses Ch. 21 Notes: Immune System I. Innate Defenses Surface defenses: Skin & mucous membranes, first line of defense Skin & mucous membranes are physical barriers to entry Protective chemicals on skin & mucous membranes Innate internal defenses: Cells & chemical defenses, 2nd line of defense Phagocytosis (neutrophils, macrophages) Natural killer cells Kill virally-infected & cancerous cells before adaptive defenses kick in Fever “Hypothalamic thermostat” resets to a higher temp Activates heat-generating & heat-conserving mechanisms Higher temp may lead to greater biochemical activity of defensive systems (but also of pathogens?) Higher temp may cause sequestration of Fe & Zn which may slow bacterial growth Inflammation Signs: heat, redness, swelling, pain – what causes these? Steps in inflammation – see figure Antimicrobial defenses Interferons Interfere with viral replication - know how Complement System of plasma proteins which, when activated, can kill target cells and can help activate other defensive systems Multiple ways to activate complement system: Classical, alternative, & lectin Adaptive Defenses Antigens Lymphocytes & antigen-presenting cells (APCs) B lymphocytes (B cells) T lymphocytes (T cells) (subtypes: helper T, cytotoxic T, regulatory T, memory T…) APCs: dendritic cells, macrophages. B cells can act as APCs. How & where do B cells & T cells develop? What are the different functions of B & T cells? Developing mymphocytes are “screened” as they mature to make sure they are immunocomptent (can recognixze & respond to antigens) and self-tolerant (i.e. do not attack body’s own tissue) Humoral Immune Response Mediated by circulating antibodies Clonal selection of B cells Only the B cell(s) that recognize the antigen are selected for proliferation (i.e. mitosis to make many copies) and differentiation (i.e. making specialized daughter cells including plasma cells and memory B cells) Role of plasma cells Role of memory B cells Primary & secondary immune responses: Why is secondary response faster & bigger? Vaccines: Work by “priming the system” or “creating a memory”, so that if/when we get infected, we have a secondary response , i.e. a big & fast response Active vs passive humaopral immunity Natural vs acquired humoral immunity Antibody structure See the figure Variable & constant regions Tips of the Y are the antigen binding sites. The 2 tips match. Five antibody classes: IgM (pentamer) first to appear in large numbers in a new response; causes agglutination IgA (dimer) mucous membranes, tears, saliva, etc. “Surface” defense IgG (monomer) most common type in plasma most of the time IgE (monomer) defense against parasitic worms; causes allergic responses IgD (monomer) on surface of B cells How antibodies help Neutralization, agglutination, precipitation, complement fixation & activation of complement system – know what these mean Cellular Immune Response Mediated by T cells CD4 cells and CD8 cells When activated, CD4 cells usually become helper Ts When activated, CD8 cells usually become cytotoxic Ts Antigen presentation and MHC proteins Class I MHC proteins found on all cells (except RBCs) in body Display antigens from within the cell – fragments of what’s inside the cell CD8 cells are activated if/when they bind to an antigen that matches their antibody, and if (only if) the CD8 molecule recognizes the presence of the MHC I protein presenting the antigen Class II MHC proteins found on APCs Present antigens from ingested foreign objects that the APC has “eaten” by phagocytosis CD4 cells are activated if/when they bind to an antigen that matches their antibody, and if (only if) the CD4 molecule recognizes the presence of the MHC II protein presenting the antigen T cell activation & differentiation See figure T cell must recognize the antigen (i.e. antigen must match the antibody on that T cell) and the T cell must recognize the MHC protein that is presenting the antigen (CD4 cell must “see” an MHC II protein; CD8 cell must “see” an MHC I protein) Co-stimulation from the APC also required for T cell activation Clonal selection of T cell: the activated T cell then divides many time by mitosis to make active daughter cells. Daughter cells differentiate to become helper Ts, regulatory Ts, memory Ts, cytotoxic Ts. Which type they become depends partly on whether the cell was a CD4 or CD8. Cytokines: chemicals that amplify the immune reposnse. Interferons, interleukins. Know what helper Ts, cytotoxic Ts, regulatory Ts do. Organ transplantation Blood easiest to transplant because RBCs don’t have MHC proteins on surface – only need to match A, B, & Rh antigens For other organs: match as many as possible of the MHC proteins. Some are more important to match than others. Autograft – from self Isograft – from identical twin Allograft – from another person, not a twin Xenograft – rom another species Immune System Challenges and Dysfunction Immunodeficiency diseases AIDS (stands for what?) Infection by HIV HIV preferentially infects & kills helper T cells Helper Ts are essential for both humoral and cellular immune responses, so knockout of helper Ts leaves patient extremely vulnerable to infection Patients often succumb to opportunistic infections (infections that wouldn’t stand a chance against a normal immune system) Severe combined immune deficiency Genetic defect (inborn error of metabolism) Hypersensitivity diseases Mounting an immune response against something that is not a major threat Immediate hypersensitivity (allergic response) Antigen binding to IgE is involved; histamine release from mast cells Subacute hypersensitivity response Delayed hypersensitivity response Autoimmune diseases Immune system attacks body’s own tissues More specifically, lymphocytes mistake body tissues for “foreign antigens” & mount an attack Type I diabetes: beta cells of the pancreas get attacked & wiped out Rheumatoid arthritis: synovial membrane of joints gets attacked & damaged & scarred Copyright © 2015, William C. Rose