BIOL 320 1 st Edition Lecture 13 Outline of Last Lecture I Internal Defenses a Tissue Injury Healing b Phagocytic Mobilization II Adaptive Defenses a Antigens b Cells of Adaptive Immune System c Humoral Immune Response d Cell Mediated Immune Response e Homeostatic Imbalance Outline of Current Lecture III Humoral Immune Response IV Acquired Immunity V Basic Antibody Structure VI Antibody Defense Mechanisms VII Monoclonal Antibodies VIII Cell Mediated Immunity IX Helper T Cell Activation X Homeostatic Imbalance XI Hodgkin s Disease XII Acute Allergic Response XIII Hypersensitivities XIV Developmental Aspects Current Lecture Humoral 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 antigen o 1 Stimulated cell forms clones with same antigen specific binding site receptor o 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 Artificially o Naturally transferred via breast milk placenta genetics o Artificially vaccine Active vs Passive o Active your own body makes a memory cell and antibodies o 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 body Basic Antibody Structure Classes of Antibodies o IgM first class released fix complement proteins o IgA secretory in mucus saliva etc in all secretions wet membranes protect against entry o IgD on surface of B lymphocytes o 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 Complex o Inactivates by Neutralization masks dangerous parts of bacterial exotoxins viruses Enhances phagocytosis Agglutination cell bound antigens Enhances phagocytosis Precipitation soluble antigens Enhances phagocytosis o 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 hybridomas o 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 treatment Cell Mediated Immunity when the problem is inside the cell T cells o T4 or CD4 or Helper TH o T8 or CD8 or Tcytotoxic o Tsuppresor Activation of Immunocompetent TC cells 1 Double recognition required o a Class I or Class II MHC produced o 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 MHC o B Cell Activation proliferate and antibody produced o Release Cytokines jumpstarts non specific immune response attracts macrophages WBCs o Stimulate proliferation of TC cells o Therefore without TH there is little immune response Ex HIV Homeostatic Imbalance Immunodeficiency o SCID Severe Combined Immuno Deficiency genetic defect damages T B cells o AIDS virus damages helper T cells susceptibility to disease cancer Autoimmune Disease o Multiple sclerosis diabetes rheumatoid arthritis lupus o Cause many could be a problem with genetics and with the cells identifying self cells Hypersensitivity o Allergies Hodgkin s Disease An acquired immunodeficiency Cancer of the B cells Leads to immunodeficiency by depressing lymph node cells Acute Allergic Response Sensitization Stage o Antigen allergen invades body o Plasma cells produce large amount of class IgE antibodies against allergen o IgE antibodies attach to mast cells in body tissues and to circulating basophils Subsequent Secondary Responses o More of same antigen invades body o 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 stimulates secretion 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 response o Ex lupus Delayed Hypersensitiviities Type IV longer response time o Ex poison ivy Developmental 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 s o Develop T H1 s develop with exposure in the environment