Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 12, Pages 8118-8125Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.12.8118
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Funding
- NCI NIH HHS [CA 108854, R01 CA067529, CA 67529, R01 CA108854] Funding Source: Medline
- NIAID NIH HHS [AI 52267, R01 AI052267, R01 AI052267-05] Funding Source: Medline
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Inflammatory bowel disease is a chronic inflammatory response of the gastrointestinal tract mediated in part by an aberrant response to intestinal microflora. Expression of IL-23 subunits p40 and p19 within cells of the innate immune system plays a central role in the development of lower bowel inflammation in response inflammatory challenge. The NF-kB subunit c-Rel can regulate expression of IL-12/23 subunits suggesting that it could have a critical role in mediating the development of chronic inflammation within the lower bowel. In this study, we have analyzed the role of c-Rel within the innate immune system in the development of lower bowel inflammation, in two well-studied models of murine colitis. We have found that the absence of c-Rel significantly impaired the ability of Helicobacter hepaticus to induce colitis upon infection of RAG-2-deficient mice, and ameliorated the ability of CD4(+)CD45RB(high) T cells to induce disease upon adoptive transfer into RAG-deficient mice. The absence of c-Rel interfered with the expression of IL-12/23 subunits both in cultured primary macrophages and within the colon. Thus, c-Rel plays a critical role in regulating the innate inflammatory response to microflora within the lower bowel, likely through its ability to modulate expression of IL-12/23 family members.
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