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目的 观察Ⅱ型胶原 (CⅡ ) 2 63 2 72段多肽氨基酸替换对类风湿关节炎 (RA)患者T细胞激活的影响 ,探讨以HLA DRβ1特异性低T细胞反应肽抑制RAT细胞激活的可能性。 方法 分离 3 9例RA患者外周血单个核细胞 (PBMC) ,与去除T细胞受体结合表位的CⅡ修饰肽共同孵育 ,检测T细胞增生情况及患者血清中的CⅡ抗体浓度 ;分析T细胞激活与CⅡ抗体形成以及与患者临床特点的关系。结果 5 6%的RA患者的T细胞在加入CⅡ 2 63 2 72原型肽和CⅡ蛋白刺激后有明显增生。在T细胞增生阳性的 2 2例RA病人中 ,68%的患者T细胞对替换第 2 68、2 69、2 70位氨基酸的CⅡ 2 63 2 72修饰肽的反应明显低于CⅡ原型肽 (P <0 0 5 )。T细胞增生与CⅡ抗体水平呈显著正相关 (r =0 5 2 9,P <0 0 1)。短病程RA患者的CⅡ特异性T细胞增生较为显著。结论 RA患者的T细胞对去除T细胞受体结合表位的CⅡ修饰肽呈低反应性 ,CⅡ特异性T细胞激活与CⅡ抗体生成有密切关系。低T细胞反应性CⅡ修饰肽可能对类风湿关节炎的T细胞激活有抑制作用
Objective To investigate the effect of amino acid substitution of collagen Ⅱ (CⅡ) 2 63 2 72 on T cell activation in patients with rheumatoid arthritis (RA) and to explore the possibility of inhibiting the activation of RAT cells by HLA DRβ1-specific low T cell reactive peptide. Methods Peripheral blood mononuclear cells (PBMCs) from 39 patients with RA were isolated and incubated with CⅡ-modified peptides with T cell receptor binding epitopes. T cell proliferation and CⅡ antibody concentrations in serum were detected. T cell activation And C Ⅱ antibody formation and the clinical features of patients. Results T cells in 56% of RA patients were significantly hyperplastic after stimulation with CⅡ 2 72 2 72 prototype peptide and C II protein. In 22 T-cell positive RA patients, the response of 68% of T cells to the CⅡ 2 72 2 72 modified peptide that replaced amino acids 682, 692, and 6970 was significantly lower than that of CⅡ prototype peptide (P <0 0 5). There was a significant positive correlation between T cell proliferation and CⅡ antibody level (r = 0 5 2 9, P 0 01). Short duration of RA patients with C Ⅱ-specific T cell proliferation was more significant. Conclusion The T cells from RA patients showed low reactivity to the CⅡ-modified peptide with T cell receptor-binding epitopes. The activation of CⅡ-specific T cells was closely related to the production of CⅡ antibody. Low T cell reactive CⅡmodified peptides may inhibit T cell activation in rheumatoid arthritis