口服Ⅱ型胶原诱导免疫耐受对佐剂性关节炎免疫病理和Th亚群的作用  

Effects of oral tolerance induced by anministration of type Ⅱcollagen on immunopathololgy and Th cell subsets of adjuvant arthritis

作　　者：朱平[1] 王彦宏[1] 冷南[1] 王树宽[1] 吴振彪[1] 解慧[1] 张惠琴[1] 樊春梅[1] 

机构地区：[1]第四军医大学西京医院临床免疫科,西安710032

出　　处：《中华风湿病学杂志》2000年第5期289-292,共4页Chinese Journal of Rheumatology

摘　　要：目的　探讨口服Ⅱ型胶原 (CⅡ )诱导的免疫耐受抑制佐剂性关节炎 (AA)过程中 ,外周淋巴组织尤其是肠相关淋巴组织 (GALT)和病变关节中免疫病理、Th细胞亚群种类及其细胞因子表达格局的改变。方法　采用免疫组织细胞化学和原位杂交等技术 ,对饲喂和未饲喂CⅡ的AA大鼠的上述器官和组织进行研究。结果　AA组大鼠外周淋巴器官 (包括GALT)和炎症关节内均有以淋巴细胞为主的炎症反应 ,这些增生活化的淋巴细胞是以分泌的IFN γ细胞为主的Th1样细胞。证明 ,AA的全身性迟发性超敏反应 (DTH)是由分泌IFN γ的Th1样细胞介导的。CⅡ治疗组大鼠其外周淋巴器官 (包括GALT)和病变关节的炎症反应比AA组明显减轻 ,增生活化的淋巴细胞是以分泌TGF β的Th3样细胞为主。证明 ,口服CⅡ能够诱导GALT产生调节性T细胞。 结论　分泌TGF β的Th3样细胞可能是口服CⅡ致耐受鼠抑制佐剂性关节炎机制的主要介导者。Objective To develop the effective therapy for rheumatoid arthritis,and study the mechanisms of oral tolerance.Methods The peripheral lymphoid tissue including gut associated lymphoid tissue (GALT) and inflammatory joints tissue samples obtained from AA rats with or without type Ⅱ (CⅡ) collagen treatment were studied by streptavidin-biotin-enzyme complex staining and hybridization in situ .Results Inflammation response dominated by lymphocytes was observed in peripheral lymphoid organs including GALT and joints in AA control rats.These proliferated and activated lymphocytes were dominated ty IFN-γ secreting T cell subset (Th1-like cells).While,in CⅡ orally tolerized animals,a marked reduction of inflammatory response,and upregulation of the inhibitory cytokine TGF-β were observed.Conclusion The inhibitory cytokine TGF-β secreting Th3 cells may play an important role in suppression of adjuvant arthritis (AA) by oral administration of CⅡ.

关 键 词：药物耐受性 类风湿性关节炎 T淋巴细胞 免疫病理 

分 类 号：R593.2[医药卫生—内科学]