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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 investigate the immunopathological features of peripheral lymphoid tissue, especially gut-associated lymphoid tissue (GALT) and diseased joints, and the types of Th cell subsets in the process of immune tolerance induced by orally administered typeⅡcollagen (CⅡ) in adjuvant arthritis (AA) And its cytokine expression pattern changes. Methods Immunohistochemistry and in situ hybridization techniques were used to study the above organs and tissues of AA rats fed with or without CⅡ. Results All of the peripheral blood lymphoid organs (including GALT) and inflammatory joints in AA group had lymphocyte predominant inflammatory reaction, and these proliferating activated lymphocytes were Th1-like cells mainly composed of secreted IFNγ cells. It was demonstrated that systemic delayed-onset hypersensitivity (DTH) in AA is mediated by Th1-like cells secreting IFNγ. The inflammatory reaction of peripheral lymphoid organs (including GALT) and diseased joints in CⅡ treated group was significantly reduced compared with that of AA group. The proliferating activated lymphocytes were mainly Th3-like cells that secreted TGFβ. It is demonstrated that oral CII can induce GALT to produce regulatory T cells. Conclusions TGFβ secreting Th3-like cells may be the main mediators of oral C Ⅱ-induced tolerance to adjuvant arthritis in rats.