BTLA associates with increased Foxp3 expression in CD4(+) T cells in dextran sulfate sodium-induced colitis

作者：Zhang Han Xian; Zhu Bin; Fu Xiao Xia; Zeng Jin Cheng; Zhang Jun Ai; Wang Wan Dang; Kong Bin; Xiang Wen Yu; Zhong Jixin; Wang Cong Yi; Zheng Xue Bao^*; Xu Jun Fa

来源：International Journal of Clinical and Experimental Pathology, 2015, 8(2): 1259.

• Colitis
• dextran sulfate sodium
• B and T lymphocyte attenuator
• Foxp3
• IL-17
• IFN-gamma

Ulcerative colitis (UC) is an inflammatory bowel disease, and its pathogenesis involves a variety of genetic, environmental, and immunological factors such as T helper cells and their secreted cytokines. B and T lymphocyte attenuator (BTLA) is an immunoregulatory receptor that has a strong suppressive effect on T-cell function. However the role of BTLA in UC remains poorly understood. Here we demonstrated that the frequency of BTLA-expressing CD3(+) T cells, especially CD4(+) T cells, increased in blood and mucosa in mice with DSS-induced colitis. The frequency of Foxp3-expressing cells in BTLA+ CD4(+) T cell from lamina propria mononuclear cells (LPMCs) was much higher in DSS-treated mice than that in controls. Similarly, the proportion of IL-17+ cells in BTLA+ CD4+ T cells from LPMCs in DSS-treated mice is much higher than that in controls, while no perceptible difference for the proportion of IFN-gamma+ cells in BTLA+ CD4(+) T cells was noted between DSS-treated mice and controls. Treatment of mesalazine, an anti-ulcerative colitis drug, down-regulated Foxp3 and IL-17 expression in BTLA positive T cells along with attenuated severity for colitis. Our findings indicate that BTLA may be involved in the control of inflammatory responses through increasing Foxp3 expression, rather than attenuating IL-17 production, in DSS-induced colitis.

• 单位
  1; 广东医学院