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CXCR3 Directs Antigen-Specific Effector CD4⁺ T Cell Migration to the Lung During Parainfluenza Virus Infection¹

Jacob E. Kohlmeier^*, Tres Cookenham^*, Shannon C. Miller^*, Alan D. Roberts^*, Jan P. Christensen, Allan R. Thomsen and David L. Woodland^2,*

^* Trudeau Institute, Saranac Lake, NY 12983; and University of Copenhagen, Institute of International Health, Immunology, and Microbiology, Copenhagen, Denmark

Effector T cells are a crucial component of the adaptive immune response to respiratory virus infections. Although it was previously reported that the chemokine receptors CCR5 and CXCR3 affect trafficking of respiratory virus-specific CD8⁺ T cells, it is unclear whether these receptors govern effector CD4⁺ T cell migration to the lungs. To assess the role of CCR5 and CXCR3 in vivo, we directly compared the migration of Ag-specific wild-type and chemokine receptor-deficient effector T cells in mixed bone marrow chimeric mice during a parainfluenza virus infection. CXCR3-deficient effector CD4⁺ T cells were 5- to 10-fold less efficient at migrating to the lung compared with wild-type cells, whereas CCR5-deficient effector T cells were not impaired in their migration to the lung. In contrast to its role in trafficking, CXCR3 had no impact on effector CD4⁺ T cell proliferation, phenotype, or function in any of the tissues examined. These findings demonstrate that CXCR3 controls virus-specific effector CD4⁺ T cell migration in vivo, and suggest that blocking CXCR3-mediated recruitment may limit T cell-induced immunopathology during respiratory virus infections.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants AI67967, AI76499, and T32 AI49823 (to D.L.W.), F32 AI71478 (to J.E.K.), and funds from the Trudeau Institute.

² Address correspondence and reprint requests to Dr. David L. Woodland, Trudeau Institute, 154 Algonquin Avenue, Saranac Lake, NY 12983. E-mail address: dwoodland{at}trudeauinstitute.org

³ Abbreviations used in this paper: BM, bone marrow; WT, wild type; BAL, bronchoalveolar lavage; MLN, mediastinal lymph node.

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The JI 2009 183: 4143-4144. [Full Text]