摘要
目的:探讨共刺激分子在桥本甲状腺炎(HT)发病中的免疫病理作用。方法:采用免疫组织化学法检测20例HT和20例甲状腺瘤旁正常组织(对照组)CD40/CD40L、B7-1/CD28、GL50、CD4和CD8分子的表达,进行分析。结果:(1)HT甲状腺滤泡细胞(TFC)B7-1表达明显高于对照组,CD40表达明显低于对照组,且有显著性差异(P<0.01);(2)HT组织浸润细胞CD28、GL50、CD4和CD8表达明显高于对照组,且有显著性差异(P<0.01),但CD40L表达无显著性差异(P>0.05)。结论:CD40/CD40L、B7/CD28、GL50等共刺激分子表达异常以及局部CD4+和CD8+/T淋巴细胞浸润异常可能与HT甲状腺滤泡细胞破坏和功能减退有关。
Objective:To investigate the role of costimulatory molecules in the immunopathogenesis of HT. tochemistry was performed to detect expression of CD40/CD40L, B7-1/CD28, GL50, CD4, and CD8 in the tissue of HT. Results:Expression levels of B7-1/CD28, GL50, CD4, and CD8 were significantly higher in the HT group than those in the control group (p 〈 0.01),while expression levels of CD40 was significantly lower in the HT group than those in the control group (p 〈 0.01).But no significant difference was found between the two groups in terms of CD40L expression (p 〉 0.05 ). Conclusion:The abnormal expressions of costimulatory molecules and infiltrated T lymphocytes seem to be related to the destruction of thyroid follicular cells and the hypofunction of thyroid in HT patients.
出处
《中国交通医学杂志》
2005年第6期584-585,共2页
Chinese Medical JOurnal of Communications
关键词
桥本甲状腺炎
共刺激分子
免疫组织化学
Hashimoto thyroiditis
Costimulatory molecule
Immunohistochemistry