The overreaction of the helper T cells and overproduction of cytokines damage tissues, cause inflammation, and cell death. Type IV hypersensitivity can usually be resolved with topical corticosteroids and trigger avoidance.[1]
Induration and erythema around injection site indicates previous exposure
An example of a tuberculosis (TB) infection that comes under control: M. tuberculosis cells are engulfed by macrophages after being identified as foreign but, due to an immuno-escape mechanism peculiar to mycobacteria,[4] TB bacteria block the fusion of their enclosing phagosome with lysosomes which would destroy the bacteria. Thereby TB can continue to replicate within macrophages. After several weeks, the immune system somehow [mechanism as yet unexplained] ramps up and, upon stimulation with interferon gamma, the macrophages become capable of killing M. tuberculosis by forming phagolysosomes and nitric oxideradicals. The hyper-activated macrophages secrete TNF-α which recruits multiple monocytes to the site of infection. These cells differentiate into epithelioid cells which wall off the infected cells, but results in significant inflammation and local damage.
^ abWarrington, Richard; Watson, Wade; Kim, Harold L.; Antonetti, Francesca Romana (10 November 2011). "An introduction to immunology and immunopathology". Allergy, Asthma & Clinical Immunology. 7 (1): S1. doi:10.1186/1710-1492-7-S1-S1. ISSN 1710-1492. PMC3245432. PMID 22165815.
^ abcdefgKumar, Vinay; Abbas, Abul K.; Aster, Jon C. (1 May 2012). Robbins Basic Pathology. Elsevier Health Sciences. ISBN978-1455737871.
^ ab"Hypersensitivity reactions". microbiologybook.org. University of South Carolina School of Medicine - Microbiology and Immunology On-line. Retrieved 29 May 2016.
^McDonough, K.; Kress, Y.; Bloom, B. R. (July 1993). "Pathogenesis of tuberculosis: interaction of Mycobacterium tuberculosis with macrophages". Infect. Immun. 61 (7): 2763–2773. doi:10.1128/iai.61.7.2763-2773.1993. eISSN 1098-5522. ISSN 0019-9567. PMC280919. PMID 8514378. S2CID 19523447. Retrieved 18 June 2017.
^Marwa, K; Kondamudi, NP (1 January 2021). "Type IV Hypersensitivity Reaction". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 32965899. Retrieved 28 November 2021.
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Type IV hypersensitivity in the Gell and Coombs classification of allergic reactions often called delayed type hypersensitivity is a type of hypersensitivity reaction that can take a day or more to develop 1 Unlike the other types it is not humoral not antibody mediated but rather is a type of cell mediated response This response involves the interaction of T cells monocytes and macrophages Type IV hypersensitivityOther namesdelayed type hypersensitivity DTH cell mediated hypersensitivitySpecialtyImmunology This reaction is caused when CD4 Th1 cells recognize foreign antigen in a complex with the MHC class II on the surface of antigen presenting cells These can be macrophages that secrete IL 12 which stimulates the proliferation of further CD4 Th1 cells CD4 T cells secrete IL 2 and interferon gamma IFNg inducing the further release of other Th1 cytokines thus mediating the immune response Activated CD8 T cells destroy target cells on contact whereas activated macrophages produce hydrolytic enzymes and on presentation with certain intracellular pathogens transform into multinucleated giant cells The overreaction of the helper T cells and overproduction of cytokines damage tissues cause inflammation and cell death Type IV hypersensitivity can usually be resolved with topical corticosteroids and trigger avoidance 1 Contents 1 Forms 2 See also 3 References 4 External linksForms editThis section needs additional citations for verification Please help improve this article by adding citations to reliable sources in this section Unsourced material may be challenged and removed May 2017 Learn how and when to remove this template message Disease Target antigen EffectsAllergic contact dermatitis 2 Environmental chemicals like urushiol from poison ivy and poison oak metals e g nickel topical medication epidermal necrosis inflammation skin rash and blistersAutoimmune myocarditis 2 Myosin heavy chain protein CardiomyopathyDiabetes mellitus type 1 2 Pancreatic beta cell proteins possibly insulin glutamate decarboxylase Insulitis beta cell destructionGranulomas 3 Various depending on underlying disease Walled off lesion containing macrophages and other cellsSome peripheral neuropathies Schwann cell antigen Neuritis paralysisHashimoto s thyroiditis 2 Thyroglobulin antigen Hypothyroidism hard goiter follicular thymitisInflammatory bowel disease 2 Enteric microbiota and or self antigens Hyperactivation of T cells cytokine release recruitment of macrophages and other immune cells inflammationMultiple sclerosis 2 Myelin antigens e g myelin basic protein Myelin destruction inflammationRheumatoid arthritis 2 Possibly collagen and or citrullinated self proteins Chronic arthritis inflammation destruction of articular cartilage and boneTuberculin reaction Mantoux test 3 Tuberculin Induration and erythema around injection site indicates previous exposureAn example of a tuberculosis TB infection that comes under control M tuberculosis cells are engulfed by macrophages after being identified as foreign but due to an immuno escape mechanism peculiar to mycobacteria 4 TB bacteria block the fusion of their enclosing phagosome with lysosomes which would destroy the bacteria Thereby TB can continue to replicate within macrophages After several weeks the immune system somehow mechanism as yet unexplained ramps up and upon stimulation with interferon gamma the macrophages become capable of killing M tuberculosis by forming phagolysosomes and nitric oxide radicals The hyper activated macrophages secrete TNF a which recruits multiple monocytes to the site of infection These cells differentiate into epithelioid cells which wall off the infected cells but results in significant inflammation and local damage Some other clinical examples Urushiol induced contact dermatitis 5 Chronic transplant rejection Coeliac disease Giant cell arteritis Graft versus host disease 6 LeprosySee also editHypersensitivity Type I hypersensitivity Type II hypersensitivity Type III hypersensitivityReferences edit a b Warrington Richard Watson Wade Kim Harold L Antonetti Francesca Romana 10 November 2011 An introduction to immunology and immunopathology Allergy Asthma amp Clinical Immunology 7 1 S1 doi 10 1186 1710 1492 7 S1 S1 ISSN 1710 1492 PMC 3245432 PMID 22165815 a b c d e f g Kumar Vinay Abbas Abul K Aster Jon C 1 May 2012 Robbins Basic Pathology Elsevier Health Sciences ISBN 978 1455737871 a b Hypersensitivity reactions microbiologybook org University of South Carolina School of Medicine Microbiology and Immunology On line Retrieved 29 May 2016 McDonough K Kress Y Bloom B R July 1993 Pathogenesis of tuberculosis interaction of Mycobacterium tuberculosis with macrophages Infect Immun 61 7 2763 2773 doi 10 1128 iai 61 7 2763 2773 1993 eISSN 1098 5522 ISSN 0019 9567 PMC 280919 PMID 8514378 S2CID 19523447 Retrieved 18 June 2017 Marwa K Kondamudi NP 1 January 2021 Type IV Hypersensitivity Reaction StatPearls Treasure Island FL StatPearls Publishing PMID 32965899 Retrieved 28 November 2021 Walter Duane Hinshaw 26 June 2021 eMedicine Hypersensitivity Reactions Delayed External links edit Retrieved from https en wikipedia org w index php title Type IV hypersensitivity amp oldid 1193828044, wikipedia, wiki, book, books, library,
