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Type 1 and 2 T helper cell-mediated colitis

Dohi, Taekoa; Fujihashi, Kohtarob

Current Opinion in Gastroenterology: November 2006 - Volume 22 - Issue 6 - p 651–657
doi: 10.1097/01.mog.0000245545.80160.0f

Purpose of review Abrogation of mucosal T cell homeostasis by exaggerated not only T helper 1, but also T helper 2 cells is a major problem that leads to intestinal inflammation. In this regard, it is important to understand these different aspects of mucosal inflammation.

Recent findings Both T helper 1 and 2 cells play central roles in the induction of mucosal immune responses including secretory IgA antibody production, which would be the most beneficial aspect for the host defense mechanism. T helper 1- and 2-type responses, however, exhibit other roles in the abrogation of intestinal homeostasis. Although it has been shown that T helper 1-type immune responses are key players in the induction of intestinal inflammation in mice colitis models and also in inflammatory bowel diseases in humans, studies in murine colitis models clearly show that T helper 2-type responses are also involved in the pathophysiology of the intestinal inflammation. Both regulatory type T cells and T helper 17 cells are involved to down- or upregulate aberrant T helper 1 and 2 cell responses.

Summary Understanding the cellular and molecular mechanisms of crosstalk among T helper 1, 2, 17 and T regulatory 1 cells is central for the prevention or treatment of inflammatory bowel diseases.

aDepartment of Gastroenterology, Research Institute, International Medical Center of Japan, Tokyo, Japan

bDepartments of Pediatric Dentistry and Microbiology, Immunobiology Vaccine Center, University of Alabama at Birmingham, Birmingham, Alabama, USA

Correspondence to Dr Kohtaro Fujihashi, Department of Pediatric Dentistry, Immunobiology Vaccine Center, University of Alabama at Birmingham, 761 Bevill Biomedical Research Building, 845 19th Street South, Birmingham, AL 35294-2170, USA Tel: +1 205 934 1951; fax: +1 205 975 4436; e-mail:

© 2006 Lippincott Williams & Wilkins, Inc.