Journal
JOURNAL OF IMMUNOLOGY
Volume 181, Issue 11, Pages 7985-7993Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.11.7985
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Funding
- National Institutes of Health [R01 AI067309]
- NEI [EY12190]
- [P20 RR017703]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR017703] Funding Source: NIH RePORTER
- NATIONAL EYE INSTITUTE [P30EY012190] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI007633, R01AI067309] Funding Source: NIH RePORTER
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The chemokine, CXCL10, chemotactic for NK cells, activated T cells, and dendritic cells is highly expressed during viral infections, including HSV-1. The importance of this chemokine to the control of HSV-1 infection was tested using mice deficient in CXCL10 (CXCL10(-/-)). Following corneal infection, HSV-1 viral titers were elevated in the nervous system of CXCL10(-/-) mice, which correlated with defects in leukocyte recruitment including dendritic cells, NK cells, and HSV-1-specific CD8(+) T cells to the brain stem. In the absence of NK cells and HSV-1-specific CD8(+) T cells in wild-type (WT) or CXCL10(-/-) mice, similar levels of virus were recovered in the nervous system, suggesting these cells are responsible for the observed defects in the control of viral replication in CXCL10(-/-) mice. Leukocyte mobilization was also compared between WT, CXCL10(-/-), and mice deficient in the only known receptor for CXCL10, CXCR3 (CXCR3(-/-)). NK cell mobilization was comparably reduced in both CXCL10(-/-) and CXCR3(-/-) mice relative to WT animals. However, the reduction in mobilization of HSV-1-specific CD8(+) T cells in CXCL10(-/-) was not observed in CXCR3(-/-) mice following HSV-1 infection. The defect was not the result of an alternative receptor for CXCL10, as Ag-specific CD8(+) T cell recruitment was not reduced in mice which were deficient in both CXCL10 and CXCR3. Thus, CXCL10 deficiency results in reduced mobilization of HSV-1-specific CD8(+) T cells as a result of dysregulation of CXCR3 signaling. The Journal of Immunology, 2008, 181: 7985-7993.
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