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作 者:庞莉萍[1] 王丽莎[1] 郝慧琴[1] 索塔林[2] 方显峰[2] 贾俊英[2] 黄烽[1] 唐捷[2]
机构地区:[1]解放军总医院风湿科,北京100853 [2]中国科学院生物物理研究所感染与免疫中心生物大分子实验室
出 处:《中华风湿病学杂志》2008年第10期660-662,共3页Chinese Journal of Rheumatology
基 金:国家自然科学基金资助项目(30571726)
摘 要:目的研究肿瘤坏死因子(TNF)-α抑制剂依那西普(Etanercept)对强直性脊柱炎(AS)患者外周血T细胞活性的影响。方法10例健康志愿者,40例活动性AS患者,随机给予依那西普(50mg,皮下注射,每周1次)或安慰剂治疗,治疗前后分离外周血单个核细胞(PBMC),酶联免疫斑点法(ELISPOT)分别检测分泌TNF-α、白细胞介素(IL)-2、干扰素(IFN)-1的细胞数量。WST-1法检测T细胞增殖。结果依那西普治疗后,分泌TNF—α的单核细胞数量减少;抗CD3和抗CD28抗体刺激后,分泌IL-2和IFN-γ的T细胞数量减少。CD4^+CD8^+T细胞增殖没有明显变化。结论抗TNF—α的治疗降低了AS患者外周血T细胞的活性,改善了AS患者病情。Objective To study the effect of TNF-α antagonist (etanercept) treatment on the peripheral T cell reactivity of ankylosing spondylitis (AS) patients. Methods Peripheral blood mononuclear cells (PBMC) were collected from 40 patients with AS at baseline, after two and six weeks of etanercept treatment or placebo and from healthy controls. The number of cells that secret TNF-α,IL-2 and IFN-γwas respectively detected by ELISPOT. CD4^+/CD8^+ T cell proliferation was assayed with WST-1 live cell staining method. Results After 2 and 6 weeks of etanercept treatment, the number of TNF-α secreting monocytes was decreased. Although the T cell proliferation rate was not reduced, the number of T cells secreting IL-2 and IFN-γ under anti-CD3/anti-CD28 stimulation was significantly decreased. Conclusion The anti-TNF-α therapy suppresses the functions of effector T cells. The reduced T cell reactivity may contribute to the efficacy of the TNF-α antagonist therapy in AS patients.
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