Chapter 10 Hypersensitivity Disorders updated summer 2020 PDF

Chapter 10 Alterations in Immune Function Dr. Tashea S. Hilliard, Associate Professor LEARNING OBJECTIVES 1) Explain how type I, II, III, and IV hypersensitivity reactions differ according to the immune cell types involved and the mechanism of tissue injury. 2) Explain how hype...

Chapter 10 Alterations in Immune Function Dr. Tashea S. Hilliard, Associate Professor LEARNING OBJECTIVES 1) Explain how type I, II, III, and IV hypersensitivity reactions differ according to the immune cell types involved and the mechanism of tissue injury. 2) Explain how hypersensitivity disorders detected, prevented, and treated.  HYPERSENSITIVY DISORDERS Type I hypersensitivity (atopic or anaphylactic) is an immediate allergic or anaphylactic type of reaction mediated primarily by sensitized mast cells. The reaction is initiated when IgE antibodies located on the mast cell membrane are bound by antigen, with subsequent cross-linking of IgE receptors. Mast cell degranulation releases chemicals that mediate the signs and symptoms of anaphylaxis. Released histamine, kinin, prostaglandins, interleukins, and leukotrienes cause increased vascular permeability, vasodilation, hypotension, urticaria, and bronchoconstriction. Occurs within 15-30mins. Examples of type I reactions include drug reactions, rhinitis, atopic eczema, bee sting reactions, and asthma.  HYPERSENSITIVY DISORDERS Type II hypersensitivity (cytotoxic or cytolytic) occurs when antibodies are formed against antigens on cell surfaces, usually resulting in lysis of target cells. Cell lysis may be mediated by (IgM or IgG) activated complement fragments (membrane attack complex) or by phagocytic cells that are attracted to target cells by the attached antibodies. Occurs within 15-30 mins. Examples include transfusion reactions, erythroblastosis fetalis, myasthenia gravis, and hyperacute graft rejection.  HYPERSENSITIVY DISORDERS Type III hypersensitivity (Immune Complex/Arthus Reaction) reactions occur when antigen-antibody complexes are deposited in tissues and result in the activation of complement and subsequent tissue inflammation and destruction. Mediated by IgG. Antigen-antibody complexes activate the complement cascade and subsequently attract phagocytic cells to the tissue. History of persistent low-grade infections, inhalation of antigens into alveoli, and autoimmune production of antibodies may result in chronic production of antigen-antibody complexes. Occurs in 6 hours. Examples include glomerulonephritis, SLE, farmer’s lung arthritis, vasculitis.  HYPERSENSITIVY DISORDERS Type IV hypersensitivity (delayed-hypersensivity) reactions are T-cell mediated and do not require antibody production, in contrast to type I, II, and III reactions. Sensitized T cells react with altered or foreign cells and initiate inflammation in the dermal regions. Occurs in 24-48 hours. Contact dermatitis, tuberculin reactions, transplant rejection, and graft-versus-host disease, Guillain Barre disease, and Multiple Sclerosis are examples.