Wang Tian, Scully Eileen, Yin Zhinan, Kim Jung H, Wang Sha, Yan Jun, Mamula Mark, Anderson John F, Craft Joe, Fikrig Erol
Department of Internal Medicine, Section of Rheumatology, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520, USA.
J Immunol. 2003 Sep 1;171(5):2524-31. doi: 10.4049/jimmunol.171.5.2524.
West Nile (WN) virus causes fatal meningoencephalitis in laboratory mice, thereby partially mimicking human disease. Using this model, we have demonstrated that mice deficient in gammadelta T cells are more susceptible to WN virus infection. TCRdelta(-/-) mice have elevated viral loads and greater dissemination of the pathogen to the CNS. In wild-type mice, gammadelta T cells expanded significantly during WN virus infection, produced IFN-gamma in ex vivo assays, and enhanced perforin expression by splenic T cells. Adoptive transfer of gammadelta T cells to TCRdelta(-/-) mice reduced the susceptibility of these mice to WN virus, and this effect was primarily due to IFN-gamma-producing gammadelta T cells. These data demonstrate a distinct role for gammadelta T cells in the control of and prevention of mortality from murine WN virus infection.
西尼罗河（WN）病毒可在实验小鼠中引发致命性脑膜脑炎，从而部分模拟人类疾病。利用该模型，我们已证明缺乏γδ T细胞的小鼠更容易感染WN病毒。TCRδ（-/-）小鼠的病毒载量升高，病原体向中枢神经系统的传播更为广泛。在野生型小鼠中，γδ T细胞在WN病毒感染期间显著扩增，在体外实验中产生γ干扰素，并增强脾脏T细胞的穿孔素表达。将γδ T细胞过继转移至TCRδ（-/-）小鼠可降低这些小鼠对WN病毒的易感性，且这种效应主要归因于产生γ干扰素的γδ T细胞。这些数据表明γδ T细胞在控制和预防小鼠WN病毒感染致死方面具有独特作用。
