FOXP3型
白细胞介素2受体
结肠炎
免疫学
调节性T细胞
炎症性肠病
过继性细胞移植
白细胞介素21
生物
T细胞
医学
免疫系统
病理
疾病
作者
Holm H. Uhlig,Janine L. Coombes,Christian Mottet,Ana Ízcue,Claire Thompson,Andrea Fanger,Andrea Tannapfel,Jason D. Fontenot,Fred Ramsdell,Fiona M. Powrie
出处
期刊:Journal of Immunology
[American Association of Immunologists]
日期:2006-11-01
卷期号:177 (9): 5852-5860
被引量:463
标识
DOI:10.4049/jimmunol.177.9.5852
摘要
CD4+CD25+ regulatory T cells can prevent and resolve intestinal inflammation in the murine T cell transfer model of colitis. Using Foxp3 as a marker of regulatory T cell activity, we now provide a comprehensive analysis of the in vivo distribution of Foxp3+CD4+CD25+ cells in wild-type mice, and during cure of experimental colitis. In both cases, Foxp3+CD4+CD25+ cells were found to accumulate in the colon and secondary lymphoid organs. Importantly, Foxp3+ cells were present at increased density in colon samples from patients with ulcerative colitis or Crohn's disease, suggesting similarities in the behavior of murine and human regulatory cells under inflammatory conditions. Cure of murine colitis was dependent on the presence of IL-10, and IL-10-producing CD4+CD25+ T cells were enriched within the colon during cure of colitis and also under steady state conditions. Our data indicate that although CD4+CD25+ T cells expressing Foxp3 are present within both lymphoid organs and the colon, subsets of IL-10-producing CD4+CD25+ T cells are present mainly within the intestinal lamina propria suggesting compartmentalization of the regulatory T cell response at effector sites.
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