[PDF][PDF] Interleukin-23 restrains regulatory T cell activity to drive T cell-dependent colitis

A Izcue, S Hue, S Buonocore, CV Arancibia-Cárcamo… - Immunity, 2008 - cell.com
A Izcue, S Hue, S Buonocore, CV Arancibia-Cárcamo, PP Ahern, Y Iwakura, KJ Maloy…
Immunity, 2008cell.com
Summary Interleukin-23 (IL-23) is an inflammatory cytokine that plays a key role in the
pathogenesis of several autoimmune and inflammatory diseases. It orchestrates innate and
T cell-mediated inflammatory pathways and can promote T helper 17 (Th17) cell responses.
Utilizing a T cell transfer model, we showed that IL-23-dependent colitis did not require IL-17
secretion by T cells. Furthermore, IL-23-independent intestinal inflammation could develop if
immunosuppressive pathways were reduced. The frequency of naive T cell-derived Foxp3+ …
Summary
Interleukin-23 (IL-23) is an inflammatory cytokine that plays a key role in the pathogenesis of several autoimmune and inflammatory diseases. It orchestrates innate and T cell-mediated inflammatory pathways and can promote T helper 17 (Th17) cell responses. Utilizing a T cell transfer model, we showed that IL-23-dependent colitis did not require IL-17 secretion by T cells. Furthermore, IL-23-independent intestinal inflammation could develop if immunosuppressive pathways were reduced. The frequency of naive T cell-derived Foxp3+ cells in the colon increased in the absence of IL-23, indicating a role for IL-23 in controlling regulatory T cell induction. Foxp3-deficient T cells induced colitis when transferred into recipients lacking IL-23p19, showing that IL-23 was not essential for intestinal inflammation in the absence of Foxp3. Taken together, our data indicate that overriding immunosuppressive pathways is an important function of IL-23 in the intestine and could influence not only Th17 cell activity but also other types of immune responses.
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