O’Connor W, Kamanaka M, Booth CJ et al.A protective function for interleukin 17A in T cell-mediated intestinal inflammation. Nat Immunol 10:603-609

Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
Nature Immunology (Impact Factor: 24.97). 07/2009; 10(6):603-9. DOI: 10.1038/ni.1736
Source: PubMed

ABSTRACT Interleukin 23 (IL-23) and IL-17 have been linked to the pathogenesis of several chronic inflammatory disorders, including inflammatory bowel disease. Yet as an important function for IL-23 is emerging, the function of IL-17 in inflammatory bowel disease remains unclear. Here we demonstrate IL-17A-mediated protection in the CD45RBhi transfer model of colitis. An accelerated wasting disease elicited by T cells deficient in IL-17A correlated with higher expression of genes encoding T helper type 1-type cytokines in colon tissue. IL-17A also modulated T helper type 1 polarization in vitro. Furthermore, T cells deficient in the IL-17 receptor elicited an accelerated, aggressive wasting disease relative to that elicited by wild-type T cells in recipient mice. Our data demonstrate a protective function for IL-17 and identify T cells as not only the source but also a target of IL-17 in vivo.

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Available from: Richard A Flavell, Aug 24, 2015
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    • "Instead, RORct-dependent expression of GM-CSF from Th cells activated by IL-23 has a pivotal role in the pathogenesis; Th cell-derived GM-CSF augments the infiltration of CD45 hi CD11b + myeloid cells into CNS and contributes to the development of EAE (Codarri et al. 2011). In murine colitis models, IL-17A production from CD4 + T cells is protective because IL-17A directly suppresses the development of colitogenic Th1 cells via IL-17R expressed on activated CD4 + T cells (O'Connor et al. 2009). In contrast, as in other autoimmune disease models, IL-23 accelerates the severity of murine colitis (Ahern et al. 2010). "
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    • "Th17 cells produce IL-17 and are involved in the development of a wide range of autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, psoriasis, and inflammatory bowel disease [43]. Both protective and pathogenic effects have been described for IL-17 in distinct autoimmune diseases [44] [45]. The precise role of IL-17 in atherosclerosis is still controversial because of contradictory publications on the subject [46]. "
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    • "Quantitative real-time PCR was performed as previously described (Horsley et al., 2008; O'Connor et al., 2009). The following accession numbers were used for the Taqman primers: Mm00444241_m1 (IL- 22) and Mm00663697_m1 (IL-22Ra). "
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