NDLI: NFIL3 deficient mice develop microbiota dependent, IL-12/23 driven spontaneous colitis

Content Provider	PubMed Central
Author	Kobayashi, Taku Steinbach, Erin C. Russo, Steven M. Matsuoka, Katsuyoshi Nochi, Tomonori Maharshak, Nitsan Borst, Luke B. Bruce, Hostager Garcia Martinez, J. Victor Rothman, Paul B. Kashiwada, Masaki Sheikh, Shehzad Z. Murray, Peter J. Plevy, Scott E.
Abstract	NFIL3 (nuclear factor, IL-3 regulated) is a transcription factor that regulates multiple immunologic functions. In myeloid cells, NFIL3 is IL-10 inducible, and has a key role as a repressor of IL-12p40 transcription. NFIL3 is a susceptibility gene for the human inflammatory bowel diseases. Here we describe spontaneous colitis in Nfil3 −/− mice. Mice lacking both Nfil3 and Il10 (NIDKO) had severe early-onset colitis, suggesting NFIL3 and IL-10 independently regulate mucosal homeostasis. Lymphocytes were necessary for colitis, as Nfil3/Rag1 double knockout (NRDKO) mice were protected from disease. However, NRDKO mice adoptively transferred with wild type CD4+ T cells developed severe colitis compared to Rag1 −/− recipients, suggesting that colitis was linked to defects in innate immune cells. Colitis was abrogated in Nfil3/Il12b double-deficient mice, identifying Il12b dysregulation as a central pathogenic event. Finally, germ-free Nfil3 −/− mice do not have colonic inflammation. Thus, NFIL3 is a microbiota-dependent, IL-10-independent regulator of mucosal homeostasis via IL-12p40.
Related Links	http://dx.doi.org/10.4049/jimmunol.1301819
Ending Page	1927
Page Count	10
Starting Page	1918
File Format	PDF
ISSN	00221767
e-ISSN	15506606
Journal	Journal of immunology (Baltimore, Md. : 1950)
Issue Number	4
Volume Number	192
Language	English
Publisher Date	2014-02-15
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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