Misplaced Pages

Type IV hypersensitivity

Article snapshot taken from Wikipedia with creative commons attribution-sharealike license. Give it a read and then ask your questions in the chat. We can research this topic together.
(Redirected from Delayed hypersensitivity) Type of allergic reaction

Medical condition
Type IV hypersensitivity
Other namesdelayed-type hypersensitivity; DTH; cell-mediated hypersensitivity
SpecialtyImmunology Edit this on Wikidata

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. 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.

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 (IFNγ), 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.

Forms

This 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 message)
Disease Target antigen Effects
Allergic contact dermatitis 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 Myosin heavy chain protein Cardiomyopathy
Diabetes mellitus type 1 Pancreatic beta cell proteins (possibly insulin, glutamate decarboxylase) Insulitis, beta cell destruction
Granulomas Various, depending on underlying disease Walled-off lesion containing macrophages and other cells
Some peripheral neuropathies Schwann cell antigen Neuritis, paralysis
Hashimoto's thyroiditis Thyroglobulin antigen Hypothyroidism, hard goiter, follicular thymitis
Inflammatory bowel disease Enteric microbiota and/or self antigens Hyperactivation of T-cells, cytokine release, recruitment of macrophages and other immune cells, inflammation
Multiple sclerosis Myelin antigens (e.g., myelin basic protein) Myelin destruction, inflammation
Rheumatoid arthritis Possibly collagen and/or citrullinated self proteins Chronic arthritis, inflammation, destruction of articular cartilage and bone
Tuberculin reaction (Mantoux test) 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, 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 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-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.

Some other clinical examples:

See also

References

  1. ^ 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.
  2. ^ Kumar, Vinay; Abbas, Abul K.; Aster, Jon C. (1 May 2012). Robbins Basic Pathology. Elsevier Health Sciences. ISBN 978-1455737871.
  3. ^ "Hypersensitivity reactions". microbiologybook.org. University of South Carolina School of Medicine - Microbiology and Immunology On-line. Retrieved 29 May 2016.
  4. 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.
  5. Marwa, K; Kondamudi, NP (1 January 2021). "Type IV Hypersensitivity Reaction". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 32965899. Retrieved 28 November 2021.
  6. Walter Duane Hinshaw (26 June 2021). "eMedicine - Hypersensitivity Reactions, Delayed".

External links

ClassificationD
Hypersensitivity and autoimmune diseases
Type I/allergy/atopy
(IgE)
Foreign
Autoimmune
Type II/ADCC
Foreign
  • Hemolytic disease of the newborn
    • Autoimmune
    Cytotoxic
    "Type V"/receptor
    Type III
    (Immune complex)
    Foreign
    Autoimmune
    Type IV/cell-mediated
    (T cells)
    Foreign
    Autoimmune
    GVHD
    Unknown/
    multiple
    Foreign
    Autoimmune
    Category: