| First Author | Wang S | Year | 2008 |
| Journal | J Immunol | Volume | 181 |
| Issue | 3 | Pages | 2084-91 |
| PubMed ID | 18641347 | Mgi Jnum | J:139232 |
| Mgi Id | MGI:3807594 | Doi | 10.4049/jimmunol.181.3.2084 |
| Citation | Wang S, et al. (2008) Drak2 contributes to West Nile virus entry into the brain and lethal encephalitis. J Immunol 181(3):2084-91 |
| abstractText | Death-associated protein kinase-related apoptosis-inducing kinase-2 (Drak2), a member of the death-associated protein family of serine/threonine kinases, is specifically expressed in T and B cells. In the absence of Drak2, mice are resistant to experimental autoimmune encephalomyelitis due to a decrease in the number of cells infiltrating the CNS. In the present study, we investigated the role of Drak2 in West Nile virus (WNV)-induced encephalitis and found that Drak2(-/-) mice were also more resistant to lethal WNV infection than wild-type mice. Although Drak2(-/-) mice had an increase in the number of IFN-gamma-producing T cells in the spleen after infection, viral levels in the peripheral tissues were not significantly different between these two groups of mice. In contrast, there was a reduced viral load in the brains of Drak2(-/-) mice, which was accompanied by a decrease in the number of Drak2(-/-) CD4(+) and CD8(+) T cells in the brain following WNV infection. Moreover, we detected viral Ags in T cells isolated from the spleen or brain of WNV-infected mice. These results suggest that following a systemic infection, WNV might cross the blood brain barrier and enter the CNS by being carried by infected infiltrating T cells. |
