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Lecture

Class 19.docx

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Department
Pathology
Course Code
Pathology 3240A
Professor
Craig Hall

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Immunity and Immune Disorders – Hypersensitivity Hypersensitivity Reaction of the Immune system ­ defined as excessive or pathologix rxn of the immune system o immune response might not be adequately controlled o or inappropriately targeted against self tissue o results in tissue damage ­ causes for hypersensitivity rxns o loss of self tolerance  ▯autoimmune disease o excessive rxn to microbes and cross rxn with microbial products o rxns to environmental antigens ­ Four Types o Three humoral (antibody mediated)  Ig­E  o One T cell mediated ­ Type I Hypersensitivity rxn o Also known as:  Allergy • Immediate rxn, occurring within minutes after interaction  of the antigen and IgE bound to mast cells • Late rxn (2­8 hrs post exposure) – tissue damage o Due to cytokine effect  May result in anaphylactic rxn leading to shock and death if not  treated immedaiately  Most common ex • Rxns to [ollen, dust, animals • Food allergies • Drug allergies o Mechanism of action  First exposure • An antigen (allergen) enters body (inhalation, ingestion,  injection) • TH2­ helper T cells gets activated  ▯secretes cytokines (IL­ 4)  ▯activate B cells/plasma cells  ▯secretion of IgE and  attract eisonophils (IL­5) • IgE molecules specific for antigen become attached to mast  cells (via Fc receptor= sensitized mast cell)  Second exposure – rapid response • Allergen/IgE interaction leads to activation of mast cells  and release of mediators (vasoactive amines) from granules  Degranulation of mast cells • Histamine  ▯vasodilation, increased vascular permeability,  smooth muscle contraction, increased mucus secretion • Adenosine  ▯increased bronchoconstriction and inhibits  platelet aggregation  • Chemotactive factors for neutrophils (NCF) and  eosinophils (ECF)  Production of lipid mediator • Prostaglandins and leukotrienes  ▯severe bronchospasms,  most potent vasoactive spasmogenic agents, increased  mucin production  Cytokine production • TNF, IL4, IL5, IL113  ▯these recriot and activate leukocytes • Important for amplification of response and in late phase  reaction ­ Type II hypersensitivity reaction (antibody mediated) o Antibodies directed against target antigens, fixed on cell surfaces or orther  tissue components (ECM, basement membrane) o Antigens may be normal molecules intrinsic to cell membranes or  adsbsorbed exogenous antigens o Examples are  Autoimmune haemolytic anemia  Autoimmune thrombocytopenic purpura • Platelets targeted  Graves disease (antibodies against TSH receptor ▯ timulate thyroid   epithelial cells to secrete Thyroid Hormone▯ yperthyroidism)  Myasthenia gravis (antibodies against acetylcholine receptors  00>inhibit neuromuscular transmission)  Insulin­ resitant diabetes o Mechanisms of action  Opsonisation and phagocytosis • Ex. Automine haemolytic anemia, autoimmune  thrombocytopenic  • Cells opsonized (Coated) by IgG identified by killer cells –  cytotoxic death • Cells coated with Ig recognized by macrophages ­  phagocytosis  Complement activation and tissue inflammation, cell lysis • Goodpasture syndrome  Antibody­mediated cellul
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