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Animal Bioresource in Japan

.: Home > Animal Bioresource in Japan > 2014 > Volume 63 Number 2 > Aoi Akitsu, Shigeru Kakuta, Shinobu Saijo, Yoichiro Iwakura

Rag2-deficient IL-1 Receptor Antagonist-deficient Mice Are a Novel Colitis Model in Which Innate Lymphoid Cell-derived IL-17 Is Involved in the Pathogenesis

Aoi Akitsu, Shigeru Kakuta, Shinobu Saijo, Yoichiro Iwakura
Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
Abstract :

Il1rn−/− mice spontaneously develop arthritis and aortitis by an autoimmune mechanism and also develop dermatitis by an autoinflammatory mechanism. Here, we show that Rag2−/−Il1rn−/− mice develop spontaneous colitis with high mortality, making a contrast to the suppression of arthritis in these mice. Enhanced IL-17A expression in group 3 innate lymphoid cells (ILC3s) was observed in the colon of Rag2−/−Il1rn−/− mice. IL-17A-deficiency prolonged the survival of Rag2−/−Il1rn−/− mice, suggesting a pathogenic role of this cytokine in the development of intestinal inflammation. Although IL-17A-producing T cells were increased in Il1rn−/− mice, these mice did not develop colitis, because CD4+Foxp3+ regulatory T cell population was also expanded. Thus, excess IL-1 signaling and IL-1-induced IL-17A from ILC3s cause colitis in Rag2−/−Il1rn−/− mice in which Treg cells are absent. These observations suggest that the balance between IL-17A-producing cells and Treg cells is important to keep the immune homeostasis of the colon.

Keywords :
Colitis, IL-1, IL-17, innate lymphoid cells, regulatory Tcells

Date Deposited : 07 Apr 2015 10:12

Last Modified : 07 Apr 2015 10:12

Official URL: http://

Volume 63, Number 2, - 2014

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