作者: D. Y. Ma , M. S. Suthar , S. Kasahara , M. Gale , E. A. Clark
DOI: 10.1128/JVI.02368-12
关键词:
摘要: West Nile virus (WNV) is a RNA of the family Flaviviridae and leading cause mosquito-borne encephalitis in United States. Humoral immunity essential for protection against WNV infection; however, requirements initiating effective antibody responses infection are still unclear. CD22 (Siglec-2) expressed on B cells regulates cell receptor signaling, survival, proliferation, production. In this study, we investigated how contributes to found that knockout (Cd22(-/-)) mice were highly susceptible had increased viral loads serum central nervous system (CNS) compared wild-type (WT) mice. This was not due defect humoral immunity, as Cd22(-/-) normal WNV-specific responses. However, decreased CD8(+) T those WT These defects simply reduced cytotoxic activity or death but, rather, associated with lymphocyte migration into draining lymph nodes (dLNs) infected production chemokine CCL3 dLNs after infection, suggesting affects chemotaxis via controlling restricted but also subset splenic DCIR2(+) dendritic rapidly expand early infection. Thus, plays an role by governing