c—Jun氨基末端激酶1对杀伤性T细胞抗病毒效应的影响  

The effects of JNK1 on the responses of cytolytic T cells against viral infection

作　　者：王永芹[1] 赵利美[1] 徐擎昱[1] 王鹏鹏[1] 汪洋[1] 

机构地区：[1]南开大学医学院分子病毒与病毒免疫学实验室,天津300071

出　　处：《中华微生物学和免疫学杂志》2012年第12期1020-1025,共6页Chinese Journal of Microbiology and Immunology

基　　金：国家自然科学基金资助项目（31070803）

摘　　要：目的探讨病毒感染过程中，JNK1对杀伤性T细胞应答的调节作用。方法通过皮下途径对JNK1基因敲除小鼠（JNK1）给予鼠痘病毒（ECTV）感染，对其存活情况、靶器官（肝、脾）病毒增殖情况进行观察和检测，并与野生型（wr）小鼠进行比较；采用流式细胞技术，检测感染后不同时间点野生型（WT）小鼠和JNK1小鼠脾脏和淋巴结中细胞毒性T淋巴细胞（CTL）的变化及效应；采用ELISA方法，检测感染后wT和JNK1。小鼠脾脏淋巴细胞IFN-1和IL-4的产生情况。结果JNK1基因敲除后，小鼠对ECTV的抵抗和清除能力明显下降，表现为总体病死率增加，靶器官内病毒滴度显著增高；较之WT小鼠，JNK1小鼠感染后CTL增殖能力明显降低的同时，伴随着产生IFN-y能力的下降。结论JNK1信号在ECTV感染中，对机体的抗病毒免疫应答，包括CTL的增殖和效应，可能起到重要的调节作用。Objective To examine the role of c-Jun NH2-terminal kinase（JNK） 1 in cytolytic T lymphocyte （CTL） responses against virus infection. Methods Wild-type （WT） and JNKl-knockout （JNKI） mice were infected with ectromelia virus （ECTV） through hind footpads. Survival and virus titers in the target organs （ hver and spleen） were analyzed. Effector T ceils in the spleen and popliteal lymph nodes were determined on day 3 and 7 post-infection. Proliferation and INF-Y production of CTL were also detected. Results JNK1 deficiency caused an increased susceptibility to ECTV infection in mice,indicated by higher case fatality and viral burden in target organs. The decrease in CTL response correlated with a defect in CTL proliferation and INF-Y production. Conclusion The data suggest that JNK1 is involved in expansion of activated CTL during ECTV infection, and plays an important antiviral role in regulating the proliferation and effector function of CTL.

关 键 词：免疫应答 免疫调节 JNK 杀伤性T淋巴细胞 病毒感染 

分 类 号：R3[医药卫生—基础医学]