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The best-known subset of CD1d-dependent NKT cells expresses an invariant T-cell receptor (TCR) α chain. These are referred to as type I or invariant NKT cells (iNKT) cells. They are notable for their ability to respond in an innate-like manner to danger signals and pro-inflammatory cytokines. Once activated, they engage in effector functions within hours.
iNKT cells recognize lipid antigens presented by CD1d, a non-polymorphic major histocompatibility complex class I-like antigen presenting molecule. These cells are conserved between humans and mice.The highly conserved TCR is made of Va24-Ja18 paired with Vb11 in humans, which is specific for glycolipid antigens.[1] The best known antigen of iNKT cells is α-galactosylceramide(αGalCer), which is a synthetic form of a chemical purified from the deep sea sponge Agelas Mauritanius.[2] iNKT cells are most commonly found in the liver, but are also found in the thymus, spleen, peripheral blood, bone marrow and fat tissue. In comparison to mice, humans have fewer iNKT cells and have a wide variation in the amount of circulating iNKT cells.[1]
Currently, there are five major distinct iNKT cell subsets. These subset cells produce a difference set of cytokines once activated. The subtypes iNKT1, iNKT2 and iNKT17 mirror Th Cell subsets in cytokine production. In addition there are subtypes specialized in T follicular helper-like function and Il-10 dependent regulatory functions. [3] iNKT cells develop in the thymus, and distribute to the periphery. Once activated iNKT cells can impact the type and strength of an immune response. They engage in cross talk with other immune cells, like dendritic cells, neutrophils and lymphocytes. [4]
While iNKT cells are not very numerous, their unique properties makes them an important regulatory cell that can influence how the immune system develops.[5] They are known to play a role in chronic inflammatory diseases, like autoimmune disease, asthma and metabolic syndrome. In human autoimmune diseases, their numbers are decreased in peripheral blood. It is not clear whether this is a cause or effect of the disease. Absence of microbe exposure in early development led to increased iNKT cells and immune morbidity in a mouse model.[6]
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Ebeth
- ^ a b Brennan, Patrick J.; Brigl, Manfred; Brenner, Michael B. (2013-02-01). "Invariant natural killer T cells: an innate activation scheme linked to diverse effector functions". Nature Reviews Immunology. 13 (2): 101–117. doi:10.1038/nri3369. ISSN 1474-1733.
- ^ Kawano, T.; Cui, J.; Koezuka, Y.; Toura, I.; Kaneko, Y.; Motoki, K.; Ueno, H.; Nakagawa, R.; Sato, H. (1997-11-28). "CD1d-restricted and TCR-mediated activation of valpha14 NKT cells by glycosylceramides". Science (New York, N.Y.). 278 (5343): 1626–1629. ISSN 0036-8075. PMID 9374463.
- ^ Gapin, Laurent (2016-01-20). "Development of invariant natural killer T cells". Current Opinion in Immunology. 39: 68–74. doi:10.1016/j.coi.2016.01.001. ISSN 1879-0372. PMID 26802287.
- ^ Berzins, Stuart P.; Smyth, Mark J.; Baxter, Alan G. (2011-02-01). "Presumed guilty: natural killer T cell defects and human disease". Nature Reviews Immunology. 11 (2): 131–142. doi:10.1038/nri2904. ISSN 1474-1733.
- ^ "Invariant natural killer T cells as sensors and managers of inflammation". www.sciencedirect.com. Retrieved 2016-02-10.
- ^ Olszak, Torsten; An, Dingding; Zeissig, Sebastian; Vera, Miguel Pinilla; Richter, Julia; Franke, Andre; Glickman, Jonathan N.; Siebert, Reiner; Baron, Rebecca M. (2012-04-27). "Microbial Exposure During Early Life Has Persistent Effects on Natural Killer T Cell Function". Science (New York, N.Y.). 336 (6080): 489–493. doi:10.1126/science.1219328. ISSN 0036-8075. PMC 3437652. PMID 22442383.