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T helper 17 cell

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T helper 17 cells (Th17) Th17 helper cells are a subset of T helper cells developmentally distinct from Th1 and Th2 lineages producing interleukin 17 (IL-17).

Differentiation

Transforming growth factor beta (TGF-β), interleukin 6 (IL-6), interleukin 21 (IL-21) and interleukin 23 (IL-23) contribute to Th17 formation in mice and humans. Key factors in the differentiation of Th17 cells are, besides others, the signal transducer and the activator of transcription 3 (Stat3) and the retinoic acid receptor-related orphan receptors gamma (RORγ) and alpha (RORα).[1] The Th17 cells can alter their differentiation program ultimately giving rise to either protective or pro-inflammatory pathogenic cells. The protective and non-pathogenic Th17 cells induced by IL-6 and TGF-β are termed as Treg17 cells. The pathogenic Th17 cells are induced by IL-23 and IL-1β.[2] IL-21, produced by Th17 cells themselves, has also been shown to initiate an alternative route for the activation of Th17 populations.[3] Both interferon gamma (IFNγ) and IL-4, the main stimulators of Th1 and Th2 differentiation, respectively, have been shown to inhibit Th17 differentiation. [citation needed]

Functions

Th17 cells play a role in adaptive immunity protecting the body against pathogens. However, anti-fungal immunity appears to be limited to particular sites with detrimental effects observed.[4] Their main effector cytokines are IL-17A, IL-17F, IL-21, and IL-22.[1] Th17 cells mediate the regression of tumors in mice,[5][6] but were also found to promote tumor formation induced by inflammation of the colon in mice.[7]

Th17 cells, particularly auto-specific Th17 cells, are associated with autoimmune disease such as multiple sclerosis, rheumatoid arthritis, and psoriasis.[1] Th17 overactivation against autoantigen will cause type 3 immune complex and complement-mediated hypersensitivity. Rheumatoid arthritis or Arthus reaction belong to this category.[8]

Bone erosion caused by mature osteoclast cells is common in patients with rheumatoid arthritis. Activated T helper cells such as Th1, Th2, and Th17 are found in the synovial cavity during the time of inflammation due to rheumatoid arthritis. The known mechanisms associated with the differentiation of osteoclast precursors into mature osteoclasts involve the signaling molecules produced by immune-associated cells, as well as the direct cell to cell contact of osteoblasts and osteoclast precursors. However, it has been suggested that Th17 can also play a more major role in osteoclast differentiation via cell to cell contact with osteoclast precursors.[9][10]

Th17 cells may contribute to the development of late phase asthmatic response due to its increases in gene expression relative to Treg cells.[11]

References

  1. ^ a b c José Francisco Zambrano-Zaragoza, Enrique Jhonatan Romo-Martínez, Ma. de Jesús Durán-Avelar, Noemí García-Magallanes, Norberto Vibanco-Pérez (Aug 2014). "Th17 Cells in Autoimmune and Infectious Diseases". Int J Inflam. doi:10.1155/2014/651503. PMC 4137509.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  2. ^ Singh B, Schwartz JA, Sandrock C, Bellemore SM, Nikoopour E (2013). "Modulation of autoimmune diseases by interleukin (IL)-17 producing regulatory T helper (Th17) cells". Indian J Med Res. 138 (5): 591–4. PMID 24434314.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ Korn T; Bettelli E; Gao W; et al. (July 2007). "IL-21 initiates an alternative pathway to induce proinflammatory T(H)17 cells". Nature. 448 (7152): 484–487. doi:10.1038/nature05970. PMID 17581588. {{cite journal}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  4. ^ Vautier, S. "C-type lectins, fungi and Th17 responses". Cytokine & Growth Factor Reviews. 21 (6): 405–412. doi:10.1016/j.cytogfr.2010.10.001. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  5. ^ Muranski P; Boni A; Antony PA; et al. (July 2008). "Tumor-specific Th17-polarized cells eradicate large established melanoma". Blood. 112 (2): 362–373. doi:10.1182/blood-2007-11-120998. PMC 2442746. PMID 18354038. {{cite journal}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  6. ^ Martin-Orozco N; Muranski P; Chung Y; et al. (November 2009). "T helper 17 cells promote cytotoxic T cell activation in tumor immunity". Immunity. 31 (5): 787–798. doi:10.1016/j.immuni.2009.09.014. PMC 2787786. PMID 19879162. {{cite journal}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  7. ^ Wu S; Rhee KJ; Albesiano E; et al. (September 2009). "A human colonic commensal promotes colon tumorigenesis via activation of T helper type 17 T cell responses". Nature Medicine. 15 (9): 1016–1022. doi:10.1038/nm.2015. PMC 3034219. PMID 19701202. {{cite journal}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  8. ^ Harrington, LE; Hatton, RD; Mangan, PR; Turner, Henrietta; Murphy, Theresa L; Murphy, Kenneth M; Weaver, Casey T (2005). "Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages". Nature Immunology. 6 (11): 1023–32. doi:10.1038/ni1254. PMID 16200070Template:Inconsistent citations{{cite journal}}: CS1 maint: postscript (link)
  9. ^ Fumoto, T; Takeshita, S; Ito, M; Ikeda, K (2013). "Physiological functions of osteoblast lineage and T cell-derived RANKL in bone homeostasis". J. Bone Miner. Res. 55 (4): 830–42. doi:10.1002/jbmr.2096. PMID 24014480.
  10. ^ Won, HY; Lee, J-A; Park, ZS; et al. (2011). "Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice". PLoS ONE. 6 (3): e18168. doi:10.1371/journal.pone.0018168. PMC 3064589. {{cite journal}}: |first4= missing |last4= (help)CS1 maint: unflagged free DOI (link)
  11. ^ Singh A, Yamamoto M, Ruan J, Choi JY, Gauvreau GM, Olek S, Hoffmueller U, Carlsten C, FitzGerald JM, Boulet LP, O'Byrne PM, Tebbutt SJ. (24 Jun 2014). "Th17/Treg ratio derived using DNA methylation analysis is associated with the late phase asthmatic response". Allergy Asthma Clin Immunol. 10 (1): 32. doi:10.1186/1710-1492-10-32. PMC 4078401. PMID 24991220.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
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