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• W2100158520 endingPage "2179" @default.
• W2100158520 startingPage "2168" @default.
• W2100158520 abstract "Abstract The induction of inflammatory cytokines during respiratory viral infections contributes to both disease pathogenesis and resolution. The present studies investigated the role of the chemokine CXCL10 and its specific receptor, CXCR3, in the host response to pulmonary respiratory syncytial virus (RSV) infection. Antibody‐mediated neutralization of CXCL10 resulted in a significant increase in disease pathogenesis, including airway hyperresponsiveness (AHR), mucus gene expression, and impaired viral clearance. When the pulmonary cytokine levels were examined, only type I IFN and IL‐12p70 were significantly reduced. These latter observations were reflected in reduced dendritic cell (DC) numbers and DC maturation in the lungs of RSV‐infected mice treated with anti‐CXCL10. Neutralization of the only known receptor for CXCL10, CXCR3, resulted in similar increases in pathogenic responses. When bone marrow‐derived DC were incubated with CXCL10 and RSV, an up‐regulation of type I IFN was observed. In addition, T lymphocytes were also examined and a significant decrease in the number of RSV M2 peptide‐specific CD8 + T cells was identified. These findings highlight a previously unappreciated role for the CXCL10:CXCR3 signaling axis in RSV‐infected animals by recruiting virus‐specific T cells into the lung and promoting viral clearance." @default.
• W2100158520 created "2016-06-24" @default.
• W2100158520 creator A5002640166 @default.
• W2100158520 creator A5044790672 @default.
• W2100158520 creator A5088974704 @default.
• W2100158520 date "2008-07-24" @default.
• W2100158520 modified "2023-10-17" @default.
• W2100158520 title "CXCL10/CXCR3-mediated responses promote immunity to respiratory syncytial virus infection by augmenting dendritic cell and CD8⁺T cell efficacy" @default.
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• W2100158520 doi "https://doi.org/10.1002/eji.200838155" @default.
• W2100158520 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2743117" @default.
• W2100158520 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18624292" @default.
• W2100158520 hasPublicationYear "2008" @default.
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