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TYPE IV HYPERSENSITIVITY Type IV hypersensitivity is also known as cell mediated or delayed type hypersensitivity. The classical example of this hypersensitivity is tuberculin (Montoux) reaction (figure 5) which peaks 48 hours after the injection of antigen (PPD or old tuberculin). The lesion is characterized by induration and erythema.
Table 3 - Delayed hypersensitivity reactions Type Reaction time Clinical appearance Histology lymphocytes, followed by macrophages; edema of epidermis lymphocytes, monocytes, macrophages macrophages, epitheloid and giant cells, fibrosis Antigen and site epidermal ( organic chemicals, poison ivy, heavy metals, etc.) intradermal (tuberculin, lepromin, etc.) persistent antigen or foreign body presence (tuberculosis, leprosy, etc.)

contact

48-72 hr

eczema

tuberculin

48-72 hr

local induration

granuloma

21-28 days

hardening

Type IV hypersensitivity is involved in the pathogenesis of many autoimmune and infectious diseases (tuberculosis, leprosy, blastomycosis, histoplasmosis, toxoplasmosis, leishmaniasis, etc.) and granulomas due to infections and foreign antigens. Another form of delayed hypersensitivity is contact dermatitis (poison ivy (figure 6), chemicals, heavy metals, etc.) in which the lesions are more papular. Type IV hypersensitivity can be classified into three categories depending on the time of onset and clinical and histological presentation (Table 3). Mechanisms of damage in delayed hypersensitivity include T lymphocytes and monocytes and/or macrophages. Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells secrete cytokines which activate cytotoxic T cells and recruit and activate monocytes

interferon-gamma.Comparison of Different Types of hypersensitivity characteristics antibody antigen response time appearance histology transferred with type-I (anaphylactic) IgE exogenous 15-30 minutes weal & flare basophils and eosinophil antibody type-II (cytotoxic) IgG. Goodpasture's nephritis type-III (immune complex) IgG. hay fever fetalis. lympho-cytotoxicity and IL-2 production. The delayed hypersensitivity lesions mainly contain monocytes and a few T cells. Corticosteroids and other immunosuppressive agents are used in treatment. Table 5 . interleukin-2.and macrophages.g. granuloma This page copyright 2010.med. TNF alpha/beta. Montoux test (figure 5)) and patch test (for contact dermatitis).edu/ghaffar/hyper00. Major lymphokines involved in delayed hypersensitivity reaction include monocyte chemotactic factor. necrosis complement and neutrophils antibody SLE. farmer's lung disease type-IV (delayed type) None tissues & organs 48-72 hours erythema and induration monocytes and lymphocytes T-cells tuberculin test.htm . IgM cell surface minutes-hours lysis and necrosis antibody and complement antibody erythroblastosis examples allergic asthma. July 07. Diagnostic tests in vivo include delayed cutaneous reaction (e. IgM soluble 3-8 hours erythema and edema. poison ivy. 2010 Page maintained by Richard Hunt http://pathmicro. etc. which cause the bulk of the damage (figure 4). The Board of Trustees of the University of South Carolina This page last changed on Wednesday.sc. In vitro tests for delayed hypersensitivity include mitogenic response.

edu/mystudy/immunology/ScienceOfImmunology/Effectorfunctionof Cell-mediatedimmunity(.myweb.com/10/12/2010/hs-iv-reacciones-de-hipersensibilidad-tipoiv/#_Toc255417960 http://wenliang.uga.net/chapter%2055_%20immunopharmacology.http://epidemiologiamolecular.html http://basic-clinical-pharmacology.htm .