摘要
T细胞免疫球蛋白黏蛋白分子3(Tim-3)在CD4、CD8、NK细胞中主要发挥免疫抑制作用。研究显示,在HIV感染者、乙型和丙型肝炎患者、活动性结核病患者外周血及病变局部T细胞或NK细胞中,Tim-3表达均显著增高,而且与疾病的发生和发展密切相关。阻断Tim-3信号通路可以显著提高T细胞、NK细胞功能,并有望用于这些疾病的免疫治疗。Galectin.9/Tim-3信号通路通过促进IFN7分泌细胞和抗原特异性CIL凋亡、诱导CD4+CD25+Foxp3+CD127h调节性T细胞的增殖、诱导CD11b+Ly-6G+髓性抑制细胞产生等发挥免疫抑制的作用。此文对国内外有关Tim-3的最新研究进展进行综述。
T cell immunoglobulin mucin 3(Tim-3) shows inhibitory effects on CD4, CD8 and NK cells. In indi- viduals with HIV infection, hepatitis B and C patients and tuberculosis patients, Tim-3 expression was elevated sigrlificandy on circulating T or NK cells, or on T cells of affected tissues and was associated with occurrence and progress of the diseases. Blocking galectin-9/Tim-3 pathway results in rescue of T and NK cell function and could be a target for im- munotherapy. Galectin-9/Tim-3 pathway functions through induced apoptosis of IFN γ-secreting T cells and CTL, promotion of CD4 + CIY25 + Foxp3+ CD127low regulatory T cells and myloid-derived suppressor cell. The research progress about Tim-3 are reviewed in this article.
出处
《国际流行病学传染病学杂志》
CAS
2011年第6期407-410,共4页
International Journal of Epidemiology and Infectious Disease
基金
国家自然科学基金(81071318)