BIOL 320 1st EditionLecture 13Outline of Last Lecture I. Internal Defensesa. Tissue Injury  Healingb. Phagocytic MobilizationII. Adaptive Defensesa. Antigensb. Cells of Adaptive Immune Systemc. Humoral Immune Responsed. Cell Mediated Immune Responsee. Homeostatic ImbalanceOutline of Current Lecture III. Humoral Immune ResponseIV. Acquired ImmunityV. Basic Antibody StructureVI. Antibody Defense MechanismsVII. Monoclonal AntibodiesVIII. Cell Mediated ImmunityIX. Helper T Cell ActivationX. Homeostatic ImbalanceXI. Hodgkin’s DiseaseXII. Acute Allergic ResponseXIII. HypersensitivitiesXIV. Developmental AspectsCurrent LectureHumoral Immune Response- Antigen Challenge: first encounter between a foreign antigen and a naive immunocompetent cell- Location: spleen or other lymphoid organ (nodes)- If the lymphocyte is a B cell, then antibody production stimulated.- Stimulated B cell will undergo clonal proliferation…with same receptor for that foreign antigeno 1) Stimulated cell forms clones with same antigen-specific binding site/receptoro 2) Most clones become plasma cells (function: produce antibody)o 3) Some clones become memory cells (function: to mount immediate response on next encounter)Acquired Immunity- Naturally vs. Artificiallyo Naturally: transferred via breast milk, placenta, genetics…o Artificially: vaccine- Active vs. Passiveo Active: your own body makes a memory cell and antibodieso Passive: transfer of antibodies from other source (ex: colostrum…first milk from mother)- Vaccine:- What are the major differences of Passive Humoral Immunity?o Passive: no antigen challenge; no memory cells  protection ends when products naturally degrade in the bodyBasic Antibody Structure- Classes of Antibodies:o IgM: first class released…fix complement proteinso IgA: secretory…in mucus, saliva, etc…(in all secretions: wet membranes) --> protect against entryo IgD: on surface of B lymphocyteso IgG: 75-80% of antibodies…get passed from mom to fetus (confer passive immunity to fetus)o IgE: play role in allergies and parasitic infections…cause basophils & mast cells to release histamine- *Antibodies no NOT destroy anything but merely tag/mark antigen for destruction*Antibody Defensive Mechanisms: form complexes with antigens- Antigen-Antibody Complexo Inactivates by: Neutralization (masks dangerous parts of bacterial exotoxins; viruses)- Enhances phagocytosis Agglutination (cell-bound antigens)- Enhances phagocytosis Precipitation (soluble antigens)- Enhances phagocytosiso Fixes and activates: Complement (most of destruction is done by the complement mechanism)- Enhances phagocytosis and inflammation- Leads to cell lysis Monoclonal Antibodies- Commercially prepared pure antibodies (Ab)- Produced by hybridomaso Cell hybrids: fusion of a tumor cell & antibody cell- Proliferate indefinitely & have ability to produce a single type of antibody- Uses: research, clinical testing, & cancer treatmentCell Mediated Immunity (when the problem is inside the cell)- T cells:o T4 or CD4 or Helper THo T8 or CD8 or Tcytotoxico Tsuppresor- Activation of Immunocompetent TC cells:- 1) Double recognition requiredo a) Class I or Class II MHC producedo b) Exogenous or Endogenous antigen- 2) Co-stimulation required [situation specifics]Helper T Cell Activation (bind to antigen linked to Class II MHC)- Class II MHCo B Cell Activation  proliferate and antibody producedo Release Cytokines  jumpstarts non-specific immune response; attracts macrophages & WBCso Stimulate proliferation of TC cellso Therefore, without TH; there is little immune response Ex: HIVHomeostatic Imbalance- Immunodeficiency:o SCID (Severe Combined Immuno-Deficiency): genetic defect damages T&B cellso AIDS: virus damages helper T cells; susceptibility to disease, cancer- Autoimmune Disease:o Multiple sclerosis, diabetes, rheumatoid arthritis, lupuso Cause: many…could be a problem with genetics and with the cells identifying self cells- Hypersensitivity:o AllergiesHodgkin’s Disease- An acquired immunodeficiency- Cancer of the B cells- Leads to immunodeficiency by depressing lymph node cellsAcute Allergic Response- Sensitization Stageo Antigen (allergen) invades bodyo Plasma cells produce large amount of class IgE antibodies against allergeno IgE antibodies attach to mast cells in body tissues (and to circulating basophils)- Subsequent (Secondary) Responseso More of same antigen invades bodyo Antigen combines with IgE attached to mast cells (and basophils), which triggers degranulation and release of histamine (and other chemicals)o Histamine causes blood vessels to dilates and become leaky, which promotes edema; stimulatessecretion of large amounts of mucus; and causes smooth muscles to contract (if respiratory system is site of antigen entry, asthma may ensue)Hypersensitivities- Subacute: IgMs…occur in 1-3hours…last half a day (10+ hours)o Ex: mismatched blood transfusion- Immune Complex (Type III): body wide (systemic) insoluble complexes…cannot be cleared immediately so tissue responseo Ex: lupus- Delayed Hypersensitiviities (Type IV): longer response timeo Ex: poison ivyDevelopmental Aspects- 9th Week: immune stem cells are already developed in spleen and liver- Stem cells from?: bone marrow- Lymphocytes?: bone marrow & thymus- Helper Ts?:o Born with T(H2)so Develop T(H1)s…develop with exposure in the