TLR4介导HSP70BCG诱导的小鼠骨髓树突状细胞分泌IL-12

目的观察TLR4（Toll—likereceptor4）在卡介苗来源的热休克蛋白70（heat shock protein 70，HSP70DCG）冲激的小鼠骨髓来源树突状细胞（dendritic cells，DCs）的IL-12分泌的作用。方法用rmGM—CSF和rmIL-4诱导小鼠骨髓来源的DCs，在HSP70BCG冲激前加入抗TLR4抗体，用流式细胞仪检测DCs的CIM0和CD86表达；用ELISA法检测DCs上清液中的IL-12和脾T细胞上清液中的IL-2浓度。结果抗TLR4抗体对CIMO和CD86的表达无明显影响，但明显抑制DCs分泌IL-12并进而抑制DCs致敏的脾细胞分泌IL-2。结论HSP70BCG可通过TLR4途径诱导DCs分泌IL-12。

Heat shock protein 70 from BCG induces marrow-derived dendritic cell to secret IL-12 through TLR4

Objective To observe the roles of toll-like receptor 4 (TLR 4) in secretion of IL-12 from bone marrow-derived dendritic cells (DCs) of mice. Methods DCs were cultured in medium containing recombinant mouse GM-CSF and IL-4. DCs treated with anti-TLR4 monoclonal antibody for 30 minutes previously were pulsed with HSP70_ BCG . Expressions of CD40 and CD86 by DCs were measured by flow cytometry. Concentration of IL-12 in supernatant of DCs cultures and IL-2 in supernatant of spleen T lymphocytes primed with DCs were measured with ELISA. Results Anti-TLR4 monoclonal antibody did not change the expressions of CD40 and CD86 induced by HSP70_ BCG , but inhibited the secretion of IL-12 from DCs and IL-2 from T lymphocytes primed with DCs pulsed with HSP70_ BCG . Conclusion HSP70_ BCG induces IL-12 secretion from DCs through TLR4.