Microbiology

                                         

                                         Overview of Hypersensitivity Reactions

·                         Altered reaction to an Ag that results in pathologic reactions upon the exposure of a sensitized host to that Ag

·                         Not necessarily an “over-reactive” immune response, but an inappropriate one (“abnormally active”)

·                         Both endogenous and exogenous Ag may elicit hypersensitivity reactions

·                         The development of hypersensitivity diseases is often associated with the inheritance of particular susceptibility genes. 

·                         All reaction types have a sensitization phase and effector phase

·                         Hypersensitivity reflects an imbalance between the effector mechanisms of immune responses and the control mechanisms that serve to normally limit such responses.

·                         Four types based on the mechanism by which immune reactions initiate tissue injury

·                         Increasingly recognized that multiple mechanisms may be operative in any one hypersensitivity disease and some disease represent a continuum of reaction types.

Type	Prototype Disorder	Immune Mechanisms	Pathologic Lesions
Type I hypersensitivity (immediate)	Anaphylaxis; allergies; bronchial asthma (atopic forms)	Production of IgE antibody → immediate release of vasoactive amines and other mediators from mast cells; recruitment of inflammatory cells (late-phase reaction)	Vascular dilation, edema, smooth muscle contraction, mucus production, inflammation
Type II hypersensitivity	IMHA; Good pasture syndrome	Production of IgG, IgM → binds to antigen on target cell or tissue → phagocytosis or lysis of target cell by activated complement or Fc receptors; recruitment of leukocytes	Cell lysis; inflammation
Type III hypersensitivity (immune complex- mediated)	SLE; some forms of glomerulonephritis; serum sickness; Arthus reaction	Deposition of antigen-antibody complexes → complement activation → recruitment of leukocytes by complement products and Fc receptors → release of enzymes and other toxic molecules	Necrotizing vasculitis (fibrinoid necrosis); inflammation
Cell-mediated (type IV) hypersensitivity	Contact dermatitis; multiple sclerosis; type I, diabetes; transplant rejection; tuberculosis	Activated T lymphocytes → i) release of cytokines and macrophage activation; ii) T cell-mediated cytotoxicity	Perivascular cellular infiltrates; edema; cell destruction; granuloma formation