Liu M T, Chen B P, Oertel P, Buchmeier M J, Armstrong D, Hamilton T A, Lane T E
Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92612, USA.
J Immunol. 2000 Sep 1;165(5):2327-30. doi: 10.4049/jimmunol.165.5.2327.
The contribution of the T cell chemoattractant chemokine IFN-inducible protein 10 (IP-10) in host defense following viral infection of the CNS was examined. IP-10 is expressed by astrocytes during acute encephalomyelitis in mouse hepatitis virus-infected mice, and the majority of T lymphocytes infiltrating into the CNS expressed the IP-10 receptor CXCR3. Treatment of mice with anti-IP-10 antisera led to increased mortality and delayed viral clearance from the CNS as compared with control mice. Further, administration of anti-IP-10 led to a >70% reduction (p </= 0.001) in CD4+ and CD8+ T lymphocyte infiltration into the CNS, which correlated with decreased (p </= 0.01) levels of IFN-gamma. These data indicate that IP-10 functions as a sentinel molecule in host defense and is essential in the development of a protective Th1 response against viral infection of the CNS.
研究了T细胞趋化因子趋化因子IFN诱导蛋白10（IP-10）在中枢神经系统病毒感染后宿主防御中的作用。在感染小鼠肝炎病毒的小鼠发生急性脑脊髓炎期间，星形胶质细胞表达IP-10，并且浸润到中枢神经系统的大多数T淋巴细胞表达IP-10受体CXCR3。与对照小鼠相比，用抗IP-10抗血清处理小鼠导致死亡率增加和病毒从中枢神经系统清除延迟。此外，给予抗IP-10导致进入中枢神经系统的CD4 +和CD8 + T淋巴细胞浸润减少> 70％（p≤0.001），这与IFN-γ水平降低（p≤0.01）相关。这些数据表明，IP-10在宿主防御中起哨兵分子的作用，并且在针对中枢神经系统病毒感染的保护性Th1反应的发展中是必不可少的。
