| First Author | Fadel SA | Year | 2008 |
| Journal | Eur J Immunol | Volume | 38 |
| Issue | 12 | Pages | 3376-87 |
| PubMed ID | 19039768 | Mgi Jnum | J:141370 |
| Mgi Id | MGI:3818184 | Doi | 10.1002/eji.200838628 |
| Citation | Fadel SA, et al. (2008) CXCR3-deficiency protects influenza-infected CCR5-deficient mice from mortality. Eur J Immunol 38(12):3376-3387 |
| abstractText | Mice lacking the chemokine receptor CCR5 are susceptible to mortality from a normally non-lethal influenza infection. Here we found that CXCR3-deficiency rescued CCR5-deficient (CCR5(-/-)) mice from influenza-induced mortality. The number of mononuclear phagocytes in the airways was transiently increased in CCR5(-/-) mice but not in CXCR3-CCR5 double-deficient mice. Antigen-specific CXCR3-CCR5 double-deficient CD8 effector cells were less efficient at entering the airways compared with WT or CCR5(-/-) CD8 effector cells. The decrease in inflammatory cell infiltrates in CXCR3-CCR5 double-deficient-infected mice correlated with a decrease in CCL2 and IFN-gamma production in the airways. Finally, CXCR3-CCR5 double-deficient mice that survived the primary viral challenge were protected from a lethal secondary challenge, indicating that T-cell-mediated protective memory was not compromised in mice lacking these chemokine receptors. In conclusion, CXCR3-deficiency attenuated the lethal cellular immune response in CCR5(-/-) influenza-infected mice without hindering viral clearance or long-term immunity. |
