Copyright
©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Sep 7, 2008; 14(33): 5110-5114
Published online Sep 7, 2008. doi: 10.3748/wjg.14.5110
Published online Sep 7, 2008. doi: 10.3748/wjg.14.5110
Role of STAT3 in inflammatory bowel disease
Ken Sugimoto, Experimental Pathology, Massachusetts General Hospital, Harvard Medical School, Boston MA 02114, United States
Author contributions: Sugimoto K contributed all to this paper.
Correspondence to: Ken Sugimoto, MD, Experimental Pathology, Massachusetts General Hospital, Harvard Medical School, Boston MA 02114, United States. sugiken@jg8.so-net.ne.jp
Telephone: +1-617-6433652 Fax: +1-617-7262365
Received: April 29, 2008
Revised: June 23, 2008
Accepted: June 30, 2008
Published online: September 7, 2008
Revised: June 23, 2008
Accepted: June 30, 2008
Published online: September 7, 2008
Abstract
Signal transducers and activators of transcription 3 (STAT3) play an important role in various autoimmune disorders including inflammatory bowel disease (IBD). Recent studies have revealed that STAT3 activation plays distinctly different roles between innate immune responses and acquired immune responses in colitis. STAT3-mediated activation of acquired immune responses plays a pathogenic role in colitis by enhancing the survival of pathogenic T cells. In contrast, STAT3-mediated activation of innate responses contributes to the suppression of colitis. This review will summarize the current understanding of the roles of STAT3 in IBD and the potential of targeting STAT3 for the treatment of IBD, emphasizing recent observations.