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Publication : Cutting edge: IFN-γR signaling in non-T cell targets regulates T cell-mediated intestinal inflammation through multiple mechanisms.

First Author  Do JS Year  2014
Journal  J Immunol Volume  192
Issue  6 Pages  2537-41
PubMed ID  24523506 Mgi Jnum  J:209920
Mgi Id  MGI:5568908 Doi  10.4049/jimmunol.1303101
Citation  Do JS, et al. (2014) Cutting edge: IFN-gammaR signaling in non-T cell targets regulates T cell-mediated intestinal inflammation through multiple mechanisms. J Immunol 192(6):2537-41
abstractText  Naive CD4 T cells transferred into lymphopenic mice undergo spontaneous proliferation and induce chronic inflammation in the intestine. Cellular mechanisms regulating the proliferative and inflammatory processes are not fully understood. In this study, we report that IFN-gamma signaling in host cells plays a major role in limiting both T cell expansion and T cell-induced intestinal inflammation. However, the role of IFN-gamma appears to differ depending on the target cells. IFN-gamma signaling in dendritic cells controls T cell expansion, whereas IFN-gamma signaling in neutrophils seems to regulate both T cell expansion and inflammation. IFN-gamma signaling in nonhematopoietic cells may control inflammation. Therefore, our results suggest novel immunoregulatory functions for IFN-gamma to orchestrate colitogenic T cell responses through its distinct action on different non-T cell target cells.
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