CXCR3 directs antigen-specific effector CD4+ T cell migration to the lung during parainfluenza virus infection.

CXCR3 directs antigen-specific effector CD4+ T cell migration to the lung during parainfluenza virus infection.
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CXCR3在parainfluenza病毒感染期间将抗原特异性效应子CD4+ T细胞迁移到肺部。

DOI:
10.4049/jimmunol.0902022
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发表时间:
2009-10-01
影响因子:
4.4
通讯作者:
Woodland, David L.
Woodland, David L.
中科院分区:
医学2区
文献类型:
--
作者:
Kohlmeier, Jacob E.;Cookenham, Tres;Miller, Shannon C.;Roberts, Alan D.;Christensen, Jan P.;Thomsen, Allan R.;Woodland, David L.

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效应T细胞是对呼吸道病毒感染的适应性免疫应答的重要组成部分。尽管先前报道趋化因子受体CCR 5和CXCR 3在呼吸道病毒特异性效应CD 8 + T细胞上表达,但尚不清楚这些受体是否支配效应CD 4 + T细胞向肺的迁移。为了评估CCR 5和CXCR 3在体内的作用,我们直接比较了副流感病毒感染期间混合骨髓嵌合小鼠中抗原特异性野生型和趋化因子受体缺陷型效应T细胞的迁移。与野生型细胞相比,CXCR 3缺陷型效应CD 4 + T细胞迁移到肺的效率低5-10倍,而CCR 5缺陷型效应T细胞迁移到肺的效率没有受损。与其在运输中的作用相反,CXCR 3对所检查的任何组织中的效应CD 4 + T细胞增殖、表型或功能没有影响。这些发现表明,CXCR 3控制病毒特异性效应CD 4 + T细胞在体内的迁移,并表明,阻断CXCR 3介导的募集可能会限制T细胞诱导的免疫病理学在呼吸道病毒感染。
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 are expressed on respiratory virus-specific effector 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 antigen-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 5-10 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.
在B淋巴细胞缺陷小鼠中对致命流感病毒感染的抗性和恢复。
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