从CD28/B7-1探讨雷公藤多甙治疗多发性肌炎的机制

Role of CD28 in polymyositis and response to TWP treatment

目的通过CD28/B7-1激活T细胞这一途径探讨雷公藤多甙治疗多发性肌炎的分子免疫学机制。方法应用免疫荧光流式细胞计检测PM患者外周血CD4+和CD8+T细胞上CD28/B7-1分子蛋白的表达;RT-PCR法检测CD28/B7-1mRNA的表达。结果PM患者外周血CD4+和CD8+T细胞明显升高,且以CD8+T为主,分子蛋白及mRNA表达增加;经TWP干预后,CD4+和CD8+T细胞数减少CD28/B7-1,CD28/B7-1表达受抑制。结论PM表现为以CD8+T细胞介导的细胞毒作用为主的细胞免疫反应异常,CD28/B7-1与PM的发病密切相关。TWP可能通过抑制CD28/B7-1的表达发挥其治疗效应。

Objective: To explore the mechanism of tripterygium wilfordii polycoside (TWP) theatment in polymyositis (PM) via the CD28/B7-1 activating T cells. Methods: By means of immunofluorescent flowcytometry the expression of CD28 and B7-1 were measured in CD4+ or CD8+ T lymphocytes. Reverse transcripition polymerase chain reaction (RT-PCR) was used to confirm the mRNA expression of CD28 and B7-1. Results: The percentage of CD4+ and CD8+ T lymphocytes were increased in PM patients and the increasing of CD8+ T cells was more prominent, accompanied with the elevated expression of CD28/B7-1. However, in TWP group, the number of T lymphocytes and the expression of CD28/B7-1 were decreased significantly. Conclusions: PM is a CD8+ cytotoxic cells mediated immune disorder. CD28/B7-1 might possess the effect of up-regulating the immune response during the disease course, providing costimulating signals for activation of T cells. PM was suppressed effectively by TWP treatment, the mechanism may be related to the suppression of CD28/B7-1 singal transduction pathway.