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'''T helper 17 cells''' ('''T<sub>h</sub>17''') are a subset of [[interleukin 17]]-producing [[T helper cells]]. They are considered developmentally distinct from T<sub>h</sub>1 and T<sub>h</sub>2 cells and are thought to play a key role in [[Autoimmunity|autoimmune disease]].<ref name="Harrington2005">{{Harvard reference
|Surname1=Harrington
|Given1=LE
|Surname2=Hatton
|Given2=RD
|Surname3=Mangan
|Given3=PR
|Surname4=others
|Year=2005
|Title=Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages
|Journal=Nature Immunology
|Volume=6
|Issue=11
|Pages=1023-32
|ID=PMID 16200070
}}</ref><ref>{{cite journal |author=Stockinger B, Veldhoen M |title=Differentiation and function of Th17 T cells |journal=Curr. Opin. Immunol. |volume=19 |issue=3 |pages=281–6 |year=2007 |pmid=17433650}}</ref>

==Differentiation==

Activation of precursor T helper cells in the presence of [[TGF beta|TGF-beta]] and [[Interleukin 6|IL-6]] is thought to drive differentiation of T<sub>h</sub>17 cells. Aside from cytokine environment, it is unclear whether any other elements of the initial activation of T<sub>h</sub>17 cells differ from those of other T helper cells. It has been suggested that [[Interleukin 23|IL-23]] is involved in the expansion of established T<sub>h</sub>17 populations, but that cytokine alone does not induce differentiation of naive T-cell precursors into that cell type.<ref name="pmid16648838">{{cite journal
|author=Bettelli E, Carrier Y, Gao W, ''et al''
|title=Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells
|journal=Nature
|volume=441
|issue=7090
|pages=235–8
|year=2006
|pmid=16648838
|doi=10.1038/nature04753
}}</ref> [[interleukin 21|IL-21]], a cytokine produced by T<sub>h</sub>17 cells themselves, has also been shown to initiate an alternative route for the activation of T<sub>h</sub>17 populations.<ref name="Korn2007">{{Harvard reference
|Surname1=Korn
|Given1=T
|Surname2=Bettelli
|Given2=E
|Surname3=Gao
|Given3=W
|Surname4=Awasthi
|Given4=A
|Surname5=Jager
|Given5=A
|Surname6=Storm
|Given6=TB
|Surname7=Oukka
|Given7=M
|Surname8=Kuchroo
|Given8=VK
|Year=2007
|Title=IL-21 initiates an alternative pathway to induce proinflammatory Th17 cells
|Journal=Nature
|Volume=448
|Issue=
|Pages=484-488
|ID=PMID 17766098
}}</ref> Both [[Interferon type II|Interferon gamma]] and [[interleukin 4|IL-4]], the main stimulators of T<sub>h</sub>1 and T<sub>h</sub>2 differentiation respectively, have been shown to negatively regulate T<sub>h</sub>17 differentiation.

==Functions==

On initial characterisation, T<sub>h</sub>17 cells were broadly implicated in autoimmune disease and auto-specific T<sub>h</sub>17 were shown to be highly pathogenic. A more natural role for T<sub>h</sub>17 cells is suggested by studies which have demonstrated preferential induction of IL-17 in cases of host infection with various bacterial and fungal species. T<sub>h</sub>17 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.

==References==
{{reflist|2}}

==External links==
There are some open access Network Protocols for studying TH17 cells at [[Nature Protocols]]:
*[http://www.natureprotocols.com/2007/08/30/th17_cells_contribute_to_uveit_2.php TH17 cells contribute to uveitis and scleritis and are inhibited by IL-27/STAT1 in the retina - Western Blot Analysis]
*[http://www.natureprotocols.com/2007/08/31/th17_cells_contribute_to_uveit_3.php TH17 cells contribute to uveitis and scleritis and are inhibited by IL-27/STAT1 in the retina - Confocal microscopy]
*[http://www.natureprotocols.com/2007/08/31/th17_cells_contribute_to_uveit_4.php TH17 cells contribute to uveitis and scleritis and are inhibited by IL-27/STAT1 in the retina - Chromatin immunoprecipitation]

{{Blood}}
{{immune_system}}

[[Category:T cells]]

[[ru:Т-хелперы 17]]
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