Communicable Ulcerative Colitis Induced by T-bet Deficiency in the Innate Immune System Export

@article{citeulike:2672229, abstract = {Summary Inflammatory bowel disease (IBD) has been attributed to overexuberant host immunity or the emergence of harmful intestinal flora. The transcription factor T-bet orchestrates inflammatory genetic programs in both adaptive and innate immunity. We describe a profound and unexpected function for T-bet in influencing the behavior of host inflammatory activity and commensal bacteria. T-bet deficiency in the innate immune system results in spontaneous and communicable ulcerative colitis in the absence of adaptive immunity and increased susceptibility to colitis in immunologically intact hosts. T-bet controls the response of the mucosal immune system to commensal bacteria by regulating TNF-[alpha] production in colonic dendritic cells, critical for colonic epithelial barrier maintenance. Loss of T-bet influences bacterial populations to become colitogenic, and this colitis is communicable to genetically intact hosts. These findings reveal a novel function for T-bet as a peacekeeper of host-commensal relationships and provide new perspectives on the pathophysiology of IBD.}, author = {Garrett, Wendy S. and Lord, Graham M. and Punit, Shivesh and Lugo-Villarino, Geanncarlo and Mazmanian, Sarkis k and Ito, Susumu and Glickman, Jonathan N. and Glimcher, Laurie H.}, citeulike-article-id = {2672229}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.cell.2007.08.017}, citeulike-linkout-1 = {http://www.sciencedirect.com/science/article/B6WSN-4PTNRXP-C/1/d0c958181962d9efbc1082ad996ed636}, day = {5}, doi = {10.1016/j.cell.2007.08.017}, journal = {Cell}, keywords = {bacterial, ibd, mice}, month = {October}, number = {1}, pages = {33--45}, posted-at = {2008-04-15 09:12:34}, priority = {2}, title = {Communicable Ulcerative Colitis Induced by T-bet Deficiency in the Innate Immune System}, url = {http://dx.doi.org/10.1016/j.cell.2007.08.017}, volume = {131}, year = {2007} }

TY - JOUR ID - citeulike:2672229 L3 - citeulike-article-id:2672229 N2 - Summary Inflammatory bowel disease (IBD) has been attributed to overexuberant host immunity or the emergence of harmful intestinal flora. The transcription factor T-bet orchestrates inflammatory genetic programs in both adaptive and innate immunity. We describe a profound and unexpected function for T-bet in influencing the behavior of host inflammatory activity and commensal bacteria. T-bet deficiency in the innate immune system results in spontaneous and communicable ulcerative colitis in the absence of adaptive immunity and increased susceptibility to colitis in immunologically intact hosts. T-bet controls the response of the mucosal immune system to commensal bacteria by regulating TNF-[alpha] production in colonic dendritic cells, critical for colonic epithelial barrier maintenance. Loss of T-bet influences bacterial populations to become colitogenic, and this colitis is communicable to genetically intact hosts. These findings reveal a novel function for T-bet as a peacekeeper of host-commensal relationships and provide new perspectives on the pathophysiology of IBD. IS - 1 JF - Cell EP - 45 TI - Communicable Ulcerative Colitis Induced by T-bet Deficiency in the Innate Immune System VL - 131 SP - 33 KW - bacterial KW - ibd KW - mice AU - Garrett, Wendy AU - Lord, Graham AU - Punit, Shivesh AU - Lugo-Villarino, Geanncarlo AU - Mazmanian, Sarkis k AU - Ito, Susumu AU - Glickman, Jonathan AU - Glimcher, Laurie PY - 2007/10/05/ UR - http://dx.doi.org/10.1016/j.cell.2007.08.017 ER -