期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 38, 期 12, 页码 3376-3387出版社
WILEY
DOI: 10.1002/eji.200838628
关键词
Chemokines; Lung inflammation; T cells; Virology
类别
资金
- National Institutes of Health [F32AI063781, 5T32AR007238-30, RO1 CA069212-13]
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.
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