雷公藤皂苷和白介素-10抑制树突状细胞诱导实验性自身免疫性甲状腺炎(英文)

目的:研究雷公藤皂苷和白介素-10(IL-10)在树突状细胞(DC)诱导实验性自身免疫性甲状腺炎(EAT)中的作用.方法:ELISA法检测甲状腺球蛋白抗体水平,TNF_β和NO分别采用生物学方法及Griess法测定,淋巴细胞增殖试验采用MTT掺入法.结果:DC能诱导EAT的发生,表现为甲状腺内出现淋巴细胞浸润并伴有血清中TgAb明显升高;但经雷公藤皂苷和IL-10处理后,DC不能诱导EAT的发生,表现为甲状腺无病理改变,血清中TgAb明显低下.同时,雷公藤皂苷组和IL-10组小鼠TNF_β活性、NO浓度和淋巴细胞增殖能力显著低于树突状细胞组(P<0.05).结论:雷公藤皂苷和IL-10能显著抑制DC诱导EAT的发生.

Tripterygium wilfordii saponins and interleukin-10 prevent induction of experimental autoimmune thyroiditis by dendritic cells

AIM: To study the roles of Tripterygium wilfordii saponins (TII) and interleukin-10 (IL-10) on dendritic cells (DC)-induced experimental autoimmune thyroiditis (EAT). METHODS: We used mice as autoimmune thyroiditis model animals and divided them into 4 groups, namely DC group, TII group, IL-10 group, and control group. The level of thyroglobulin (Tg) antibody was assayed by ELISA. TNF beta production in the cultured supernatants and nitric oxide (NO) in the serum were measured by biological activation assay and Griess reaction, respectively. Tg-stimulated proliferation of lymphocytes was detected with MTT incorporation assay. The histopathological analysis of thyroid was carried out. RESULTS: Tg-pulsed DC were able to induce EAT with increase in the concentration of TgAb in serum and lymphocytes infiltration in thyroid. After treatment with TII or IL-10, DC could not induce EAT with lower levels of TgAb and no lymphocyte infiltration. The concentration of NO in serum, TNF beta activation, and the proliferation of lymphocytes in response to thyroglobulin in TII or IL-10 group were lower than those in DC group. CONCLUSION: TII and IL-10 are able to strongly inhibit the ability of DC to induce experimental autoimmune thyroiditis.