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CXCR3-deficiency protects influenza-infected CCR5-deficient mice from mortality.

Authors: Fadel, SA  Bromley, SK  Medoff, BD  Luster, AD 
Citation: Fadel SA, etal., Eur J Immunol. 2008 Dec;38(12):3376-87.
Pubmed: (View Article at PubMed) PMID:19039768
DOI: Full-text: DOI:10.1002/eji.200838628

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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RGD Object Information
RGD ID: 4892119
Created: 2011-02-07
Species: All species
Last Modified: 2011-02-07
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.