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Type IV hypersensitivity
OMIM [1]
DiseasesDB [2]
MedlinePlus [3]
eMedicine /
MeSH {{{MeshNumber}}}

Type 4 hypersensitivity is often called delayed type hypersensitivity as a type of immunologic hypersensitivity . Unlike the other types, it is not antibody mediated but rather is a type of Cell-mediated immunity .

CD4+ helper T cells recognize antigen in a complex with Class 2 major histocompatibility complex. The antigen-presenting cells in this case are macrophages that secrete IL-12, which stimulates the proliferation of further CD4+ Th1 cells. CD4+ T cells secrete IL-2 and interferon gamma, further inducing the 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.


Disease Target antigen Effects
Diabetes mellitus type 1 Pancreatic beta cell proteins
(possibly insulin, Glutamate decarboxylase)
Multiple sclerosis Oligodendrocyte proteins
(myelin basic protein, proteolipid protein)
Rheumatoid arthritis Antigen in synovial membrane
(possibly type II collagen)
  • Chronic arthritis
  • Destruction of articular cartilage and bone, a Type III hypersensitivity (Antibodies made against IgG)
Some peripheral neuropathies Schwann cell antigen
  • Neuritis
  • Paralysis
Hashimoto's Thyroiditis Thyroglobulin antigen
Crohn's disease Unknown
Contact dermatitis Environmental chemicals, e.g. poison ivy, nickel
Mantoux test* (diagnostic) Tuberculin
Unless else specified in boxes, then ref is:[1]

* - Mantoux test not taken from [1]

An example of a TB infection that came under control: M. tuberculosis are engulfed by macrophages after being identified as foreign, but due to a self-preserving mechanism peculiar to TB it is able to block the fusion of the phagosome within which it is existing with the lysosome which would destroy it. So it can continue existing and replicating within the immune cell designed to destroy it. After several weeks, the immune system somehow [mechanism as yet unexplained] ramps up and, on stimulation with IFN-gamma, the macrophages become capable of killing M. tuberculosis by forming phagolysosomes and nitric oxide radicals. However unfortunately the hyper-activated macrophages secrete TNF which recruits multiple monocytes into the battle. These cells differentiate into epithelioid histiocytes which wall off the infected cells, but at the cost of significant inflammation and local damage.

Some other clinical examples:


  1. 1.0 1.1 Table 5-5 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology, Philadelphia: Saunders. 8th edition.
  2. eMedicine - Hypersensitivity Reactions, Delayed : Article by Walter Duane Hinshaw.

Template:Hypersensitivity and autoimmune diseases

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