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Transcript
Clinical Immunology: Protection Immune System Reaction Damage Hypersensitivity Allergy (hypersensitivity) allergy is an altered state of reactively to an antigen or hapten, hypersensitivity means a heightened reactively. Types of hypersensitivity: Type Ι hypersensitivity: IgE Mediated,Anaphylactic, Immediate (reaction with minutes ) Allergic disease Atopic disease: In people with a hereditary predisposition to produce (IgE) against common environmental antigen (Allergen). Allergy Allos Other Ergon Reactivity Molecules from outside own body ( Allergen ) Allergen: An antigen that cause allergic reaction: Breath or take in Food Dender Bee sting Mold Drugs and Medications Pollens Contact with skin Latex Lotions Soaps First exposure ͋ Sensitization ͋ Allergen Subsequent exposure : get serious Once again: Type 1 Hypersensitivity: Most allergic reaction Genetic predisposition ( Runs in families) Example: Ragweed Pollen ( Allergen): Lymph node Antigen Presenting Cell Dendritic cell Macrophage Peptides Naïve T- Helper cell THە (Never seen antigen) Primed T- Helper Diferentiation TH 2 TH 2 release cytokines such as: IL-3, IL-4,IL-5,IL-10 and others That inhibit TH 1 cell activation IL-4, IL13 with B- cell surface molecule CD40 induce isotype switching of IgM bearing B-cell resulting in production of IgE. Degranulation of Mast cells leads to release of Pro- inflammatory mediators. Degranulation f Esinophils leads to release of toxic substances Pro-inflammatory mediators: Early Phase Reaction (within minutes) Histamine: Bronchi-Smooth muscle contraction -Difficulty breathing Blood vessels-Dilation ( increase permeability )- Edema (swelling) Late Phase Reaction (8-12 hrs.) Il4, IL5, IL10, Leukotrienes: Like histamine –Smooth muscle contraction Attract more immune cells (Neutrophils, Mast cells, Esinophils) Even after allergen gone Serotonin Kinins Proteases Esinophils granules Symptoms: Mild Symptoms Sever Symptoms (Large load of allergen) hives (urticaria) eczema allergic rhinitis nose asthma increase vascular permeability Air way constriction can ۥt supply vital organs Anaphylactic Shock inflammation Treatment: Anti-Histamine Decrease vascular permeability Decrease Bronchoconstriction Anti-Histamine Block Corticosteroides Decrease inflammatory response Epinephrine (injection IM or IV) constrict blood vessels. Histamine Type II hypersensitivity: Cytotoxic hypersensitivity This type involves the death of cells bearing Ab attached to antigen , Abs are of IgG & possibly IgM classes react directly with antigen on the surface of tissue cells (SELF). Complement participate in this reaction & promote cytolysis or cytotoxic reaction. E.g. hemolytic reaction drug, allergies, autoimmune disease & allograft rejection. Drugs (eg, Penicillins) can attach to surface proteins on red blood cells and initiate antibody formation. Such autoimmune antibodies(IgG) then interact with the red blood cell surface result in hemolysis. (self)Ag-Ab Complex: Host tissue problem Mechanisms of Type II hypersensitivity: Cytotoxic mrchanism 1: Complement Small proteins Enzymatic cascade Fight infection C3a, C4a, C5a are chemotactic factors attract Neutrophils Neutrophils degranulation release enzymes : Peroxidase Myeloperoxidase Proteinase These enzymes cause RBCs lysis Hemolytic Anemia Cytotoxic Mechanism2: Complement system: Membrane Attack Complex (MAC) COOMB ۥS TEST: Cytotoxic Mechanism 3: Complement System: C3b – Opsonization- Phagocytosis ( RBC engulfed and destroyed ) Cytotoxic Mechanism 4: Ab- Dependent Cell Mediated Cytotoxicity (ADCC) (Natural Killer Cell) Non – Cytotoxic Mechanism: eg, Myasthenia Gravis Once again: Type II hypersensitivity: Ab – mediated, Generally cytotoxic – Tissue specific. Type III hypersensitivity: Antigen antibody complex form in the soluble or fluid phase of tissue or in blood & then deposit on vessel walls & glomerular membrane to interrupt normal physiological process. This lead to complement become activated & release chemotactic factors. The attracted leucocytes release enzymes possibly other agent that injure local times, e.g. Arthus reaction, auto immune reaction and glomerlonephritis. Type IV hypersensitivity: Delayed type reaction :- the cell mediated hypersensitivity reaction involved antigen sensitize T-cells which respond directly or by the release of lymphokines. e.g. dermatitis & allergies of infections. The delayed appear of an indurate & erythematus reaction which reaches a maximum at 24-48 hrs & is characterize histology by with mononuclear phagocytes & lymphocytes. The Summary of Hypersensitivity Reactions Once again: