作者: S.M. Biswas , S. Kar , R. Singh , D. Chakraborty , V. Vipat
DOI: 10.1002/JMV.21688
关键词:
摘要: Japanese encephalitis virus (JEV) induces an acute infection of the central nervous system, pathogenic mechanism which is not fully understood. To investigate host response to JEV infection, 14-day-old mice were infected via extraneural route, resulted in and death. Mice that received immune splenocyte transfer protected from infection. Pathology gene expression profiles then compared brains either succumbed or by cell transfer. undergoing progressive had increased proinflammatory cytokines, chemokines, signal transducers associated with interferon (IFN) pathway. In contrast, receiving production Th2 cytokine IL-4, IL-10, subdued IFN-gamma. We observed IL-10 be important factor determining clinical outcome Data obtained microarray analysis further confirmed quantitative RT-PCR. Together, these data suggest causes unregulated inflammatory can countered immunomodulatory cytokines survive lethal