From Wikipedia, the free encyclopedia
T helper 17 cells (Th17) are a subset of interleukin 17-producing T helper cells. They are considered developmentally distinct from Th1 and Th2 cells and are thought to play a key role in autoimmune disease.[1][2]
[edit] Differentiation
Activation of precursor T helper cells in the presence of TGF-beta and IL-6 is thought to drive differentiation of Th17 cells. Aside from cytokine environment, it is unclear whether any other elements of the initial activation of Th17 cells differ from those of other T helper cells. It has been suggested that IL-23 is involved in the expansion of established Th17 populations, but that cytokine alone does not induce differentiation of naive T-cell precursors into that cell type.[3] IL-21, a cytokine produced by Th17 cells themselves, has also been shown to initiate an alternative route for the activation of Th17 populations.[4] Both Interferon gamma and IL-4, the main stimulators of Th1 and Th2 differentiation respectively, have been shown to negatively regulate Th17 differentiation.
[edit] Functions
On initial characterisation, Th17 cells were broadly implicated in autoimmune disease and auto-specific Th17 were shown to be highly pathogenic. A more natural role for Th17 cells is suggested by studies which have demonstrated preferential induction of IL-17 in cases of host infection with various bacterial and fungal species. Th17 primarily produce two main members of the IL-17 family; IL-17A and IL-17F which are involved in the recruitment, activation and migration of neutrophils.
[edit] References
- ^ Harrington, LE; RD Hatton & PR Mangan et al. (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, PMID 16200070
- ^ Stockinger B, Veldhoen M (2007). "Differentiation and function of Th17 T cells". Curr. Opin. Immunol. 19 (3): 281–6. PMID 17433650.
- ^ Bettelli E, Carrier Y, Gao W, et al (2006). "Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells". Nature 441 (7090): 235–8. doi:10.1038/nature04753. PMID 16648838.
- ^ Korn, T; E Bettelli & W Gao et al. (2007), "IL-21 initiates an alternative pathway to induce proinflammatory Th17 cells", Nature 448: 484-488, PMID 17766098
[edit] External links
There are some open access Network Protocols for studying TH17 cells at Nature Protocols:
