Type 1 and 2 T helper cell-mediated colitis

被引:13
|
作者
Dohi, Taeko
Fujihashi, Kohtaro
机构
[1] Univ Alabama, Dept Pediat Dent, Immunobiol Vaccine Ctr, Birmingham, AL 35294 USA
[2] Int Med Ctr Japan, Res Inst, Dept Gastroenterol, Tokyo, Japan
[3] Univ Alabama, Dept Microbiol, Immunobiol Vaccine Ctr, Birmingham, AL 35294 USA
关键词
colitis; mucosal inflammation; T helper 1 cell; T helper 2 cell;
D O I
10.1097/01.mog.0000245545.80160.0f
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
引用
收藏
页码:651 / 657
页数:7
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