Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity.
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2009Access:
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Sutton, C.E., Lalor, S.J., Sweeney, C.M., Brereton, C.F., Lavelle, E.C. and Mills, K.H.G, Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity., Immunity, 31, 2, 2009, 331-341Download Item:
interleukin-1.pdf (Accepted for publication (author's copy) - Peer Reviewed) 695.2Kb
Abstract:
Th17 cells, CD4(+) T cells that secrete interleukin-17 (IL-17), are pathogenic in autoimmune diseases and their development and expansion is driven by the cytokines IL-6, TGF-beta, IL-21, IL-1, and IL-23. However, there are also innate sources of IL-17. Here, we show that gamma delta T cells express IL-23R and the transcription factor ROR gamma t and produce IL-17, IL-21, and IL-22 in response to IL-1 beta and IL-23, without T cell receptor engagement. IL-17-producing gamma delta T cells were found at high frequency in the brain of mice with experimental autoimmune encephalomyelitis (EAE). gamma delta T cells activated by IL-1 beta and IL-23 promoted IL-17 production by CD4(+) T cells and increased susceptibility to EAE, suggesting that gamma delta T cells act in an amplification loop for IL-1 7 production by Th17 cells. Our findings demonstrate that gamma delta T cells activated by IL-1 beta and IL-23 are an important source of innate IL-17 and IL-21 and provide an alternative mechanism whereby IL-1 and IL-23 may mediate autoimmune inflammation.
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http://people.tcd.ie/lavelleehttp://people.tcd.ie/millsk
http://people.tcd.ie/lalorst
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PUBLISHEDPMID: 19682929
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Immunity31
2
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CYTOKINE, INFLAMMATION, GROWTH-FACTOR-BETA, PROINFLAMMATORY IL-17(+), MULTIPLE-SCLEROSIS, T(H)17 CELLS, TGF-BETASubject (TCD):
Immunology, Inflammation & InfectionDOI:
http://dx.doi.org/10.1016/j.immuni.2009.08.001Licences: