摘要
目的研究重组人肿瘤坏死因子受体融合蛋白(rhT-NFR:Fc)体外用药对佐剂性关节炎(AA)大鼠T淋巴细胞增殖及T细胞亚群比例的影响。方法完全弗氏佐剂(CFA)免疫SD大鼠诱导AA模型,分离培养胸腺及肠系膜淋巴结淋巴细胞,rhTNFR:Fc(10、1、0.1、0.01、0.001μg/ml)体外给药,氚标记的胸腺嘧啶核苷(3H-TdR)掺入法检测rhTNFR:Fc对胸腺T淋巴细胞增殖的影响,流式细胞术检测总Th细胞(CD4+/CD3+)、活化Th细胞(CD4+/CD25+)、CD4+/CD25+/Foxp3+Treg细胞及CD4+/CD62L+未活化Th细胞比例。结果 rhTNFR:Fc组能不同程度的抑制胸腺T淋巴细胞的异常增殖,对CD4+/CD3+总Th细胞比例无显著影响,可以明显降低异常活化的CD4+/CD25+Th细胞比例(P<0.01,P<0.05),明显提高下降的CD4+/CD25+/Foxp3+Treg细胞、CD4+/CD62L+未活化Th细胞比例(P<0.05,P<0.01)。结论 rhTNFR:Fc对AA大鼠的治疗作用可能与其抑制T淋巴细胞增殖、调节T细胞亚群比例有关。
Abstract Objective To investigate the effects of rhTNFR ： Fc on the proliferation and differentiation of T lympho- cytes from adjuvant arthritis （AA） rats. Methods AA rats were induced by complete Freund adjuvant, and thy- mocytes and T lymphocytes in lymph nodes were collected and incubated. RhTNFR： Fc （10,1,0. 1,0. 01,0. 001μg/ml） was added into the T lymphocytes suspension. Results RhTNFR： Fc could inhibit T lymphocytes prolifer- ation, down-regulated CD4^＋ CD25^＋ T cells and up-regulated unactived CD4^＋ CD62L^＋ T cells, CD4 ^＋/CD25^＋ / Foxp3^＋ Treg, but had no obvious effect on the percentage of CD3^＋ CD4^＋ T cells. Conclusion Our results indicate that rhTNFR： Fc significantly inhibits T lymphocytes proliferation and regulates T lymphocytes subtype, which might be one of the therapeutic mechanisms for rhTNFR： Fc.
出处
《安徽医科大学学报》
CAS
北大核心
2012年第11期1324-1328,共5页
Acta Universitatis Medicinalis Anhui
基金
国家自然科学基金(编号:30973543、81173075)
安徽省高校自然科学基金(编号:KJ2011Z181、KJ2011Z180)
安徽省自然科学基金(编号:1208085QH146)
