Acta pharmacologica Sinica · 2000
Tripterygium wilfordii saponins and interleukin-10 prevent induction of experimental autoimmune thyroiditis by dendritic cells.
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Wang S J, Xu H X, Liu G Z
Аннотация
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.
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.