Involves th2 and b cell class switch symptoms

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- Involves TH2 and B-cell class switch) - Symptoms: Systemic Itching Hives Skin erythemia Respiratory difficulty Pulmonary bronchoconstriction Hypersecretion of mucous Laryngeal edema Vomiting, abdominal cramps, diarrhea: Gastrointestinal contraction Drop in blood pressure (anaphylactic shock): Systemic vasodilation Type II – Antibody-mediated (IgG and IgM antibodies directed to cellular antigens) - Directed to normal cell or tissue antigens or cell surface or tissue matrix molecules that have been modified by chemical or microbial proteins. - Antibodies (IgM and IgG) directed against tissue antigens - Cell death and tissue damage Activation of the complement system: Targeting cells for phagocytosis and Inflammation Interfere with normal function: Block or change the function of the antigen they have bound to Eg. Type III – Immune complex-mediated (Circulating IgG and IgM form complexes with antigen and are deposited) - Immune complexes are formed between antibody and antigen - Exogenous antigen: Microbial protein - Endogenous protein: Nucleoprotein 4. Tissue that’s too big for phagocytosis may be damaged by antibody- dependent cell mediated cytotoxicity (ADCC) 2. Phagocytosis by macrophages and neutrophils: Antibodies recognized by Fc receptors Complement recognized by C3b receptor 3. Neutrophils release enzymes and ROS which damage tissue
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- Includes some of the most common immunologic diseases - Under normal circumstances, immune complexes are removed from circulation by the action of complement ⟹ C3b deposited on immune complex ⟹ the new complex binds to CR1 receptors on erythrocytes ⟹ removed by phagocytic cells in spleen and liver. - Immune complexes cause disease when they are produced in large amounts – persistent infection, autoimmune disease, constant environmental exposure inadequately cleared – limited Fc receptors deposit in tissue (basement membranes of blood vessels, kidney, joints) induce inflammatory reaction - Systemic: immune complexes formed in the circulation and deposited in many tissues Eg Systemic lupus erythematosus (SLE) Multi-system autoimmune disease Failure to maintain self-tolerance large array of autoantibody Clinical manifestation: Unpredictable, Remitting, Relapsing, Acute, Insidious Effects any organ through deposition of immune complexes in basement membrane: Skin, kidney, serosal membranes, joints, heart - Localized: immune complexes are deposited in specific tissues Type IV – T cell-mediated (CD4 and CD8 T-cells and macrophages) - AKA Delayed type hypersensitivity (DTH) - Due to persisting antigen specific T cells (CD4 or CD8) - Triggered by intracellular antigen - CD4 T cell mediated Recruitment of macrophages When the organism, or stimulating agent persists, macrophages and T cells accumulate at the antigen site in large numbers and result in pathology Tuberculin Reaction In individuals previously sensitized to tubercle bacillus: Vaccination or infection Tuberculin (M. tuberculosis peptides and carb)
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  • Fall '19
  • autoimmune disease

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