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Interleukin-23 drives intestinal inflammation through direct activity on T cells.

Abstract：

:Mutations in the IL23R gene are linked to inflammatory bowel disease susceptibility. Experimental models have shown that interleukin-23 (IL-23) orchestrates innate and T cell-dependent colitis; however, the cell populations it acts on to induce intestinal immune pathology are unknown. Here, using Il23r(-/-) T cells, we demonstrated that T cell reactivity to IL-23 was critical for development of intestinal pathology, but not for systemic inflammation. Through direct signaling into T cells, IL-23 drove intestinal T cell proliferation, promoted intestinal Th17 cell accumulation, and enhanced the emergence of an IL-17A(+)IFN-gamma(+) population of T cells. Furthermore, IL-23R signaling in intestinal T cells suppressed the differentiation of Foxp3(+) cells and T cell IL-10 production. Although Il23r(-/-) T cells displayed unimpaired Th1 cell differentiation, these cells showed impaired proliferation and failed to accumulate in the intestine. Together, these results highlight the multiple functions of IL-23 signaling in T cells that contribute to its colitogenic activity.

journal_name

Immunity

journal_title

Immunity

authors

Ahern PP,Schiering C,Buonocore S,McGeachy MJ,Cua DJ,Maloy KJ,Powrie F

doi

10.1016/j.immuni.2010.08.010

subject

Has Abstract

pub_date

2010-08-27 00:00:00

pages

279-88

issue

2

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(10)00293-1

journal_volume

33

pub_type

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