CAJ | 학술논문

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(WT)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-γ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-γ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.
목적 탐토병독감염과정중,JNK1대살상성T세포응답적조절작용.방법 통과피하도경대JNK1기인고제소서(JNK1-/-)급여서두병독(ECTV)감염,대기존활정황、파기관(간、비)병독증식정황진행관찰화검측,병여야생형(WT)소서진행비교；채용류식세포기술,검측감염후불동시간점야생형(WT)소서화JNK1-/-소서비장화림파결중세포독성T림파세포(CTL)적변화급효응；채용ELISA방법,검측감염후WT화JNK1-/-소서비장림파세포IFN-γ화IL-4적산생정황.결과 JNK1기인고제후,소서대ECTV적저항화청제능력명현하강,표현위총체병사솔증가,파기관내병독적도현저증고；교지WT소서,JNK1-/-소서감염후CTL증식능력명현강저적동시,반수착산생IFN-γ능력적하강.결론 JNK1신호재ECTV감염중,대궤체적항병독면역응답,포괄CTL적증식화효응,가능기도중요적조절작용.
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 JNK1-knockout (JNK1-/-) mice were infected with ectromelia virus(ECTV) through hind footpads.Survival and virus titers in the target organs (liver and spleen) were analyzed.Effector T cells in the spleen and popliteal lymph nodes were determined on day 3 and 7 post-infection.Proliferation and INF-γ 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-γproduction.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.