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 hypersensitivity | |
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Other names | delayed-type hypersensitivity; DTH; cell-mediated hypersensitivity |
Specialty | Immunology |
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 (IFN
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]
Forms
editThis section needs additional citations for verification. (May 2017) |
Disease | Target antigen | Effects |
---|---|---|
Allergic 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 blisters |
Autoimmune myocarditis[2] | Myosin heavy chain protein | Cardiomyopathy |
Diabetes mellitus type 1[2] | Pancreatic beta cell proteins (possibly insulin, glutamate decarboxylase) | Insulitis, beta cell destruction |
Granulomas[3] | Various, depending on underlying disease | Walled-off lesion containing macrophages and other cells |
Some peripheral neuropathies | Schwann cell antigen | Neuritis, paralysis |
Hashimoto's thyroiditis[2] | Thyroglobulin antigen | Hypothyroidism, hard goiter, follicular thymitis |
Inflammatory bowel disease[2] | Enteric microbiota and/or self antigens | Hyperactivation of T-cells, cytokine release, recruitment of macrophages and other immune cells, inflammation |
Multiple sclerosis[2] | Myelin antigens (e.g., myelin basic protein) | Myelin destruction, inflammation |
Rheumatoid arthritis[2] | Possibly collagen and/or citrullinated self proteins | Chronic arthritis, inflammation, destruction of articular cartilage and bone |
Tuberculin reaction (Mantoux test)[3] | Tuberculin | 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 oxide radicals. The hyper-activated macrophages secrete TNF-
Some other clinical examples:
See also
editReferences
edit- ^ a b Warrington, 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. 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".