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

Jacob E Kohlmeier; Tres Cookenham; Shannon C Miller; Alan D Roberts; Jan P Christensen; Allan R Thomsen; David L Woodland

doi:10.4049/jimmunol.0902022

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

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

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

103 Citationer (Scopus)

Abstract

Udgivelsesdato: 2009-Sep-4

Originalsprog	Engelsk
Tidsskrift	Journal of Immunology
ISSN	0022-1767
DOI	https://doi.org/10.4049/jimmunol.0902022
Status	Udgivet - 2009

Adgang til dokumentet

10.4049/jimmunol.0902022

Citationsformater

@article{f9d45620a30511debc73000ea68e967b,

title = "CXCR3 Directs Antigen-Specific Effector CD4+ T Cell Migration to the Lung During Parainfluenza Virus Infection",

abstract = "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.",

author = "Kohlmeier, {Jacob E} and Tres Cookenham and Miller, {Shannon C} and Roberts, {Alan D} and Christensen, {Jan P} and Thomsen, {Allan R} and Woodland, {David L}",

year = "2009",

doi = "10.4049/jimmunol.0902022",

language = "English",

journal = "Journal of Immunology",

issn = "0022-1767",

publisher = "American Association of Immunologists",

}

TY - JOUR

T1 - CXCR3 Directs Antigen-Specific Effector CD4+ T Cell Migration to the Lung During Parainfluenza Virus Infection

AU - Kohlmeier, Jacob E

AU - Cookenham, Tres

AU - Miller, Shannon C

AU - Roberts, Alan D

AU - Christensen, Jan P

AU - Thomsen, Allan R

AU - Woodland, David L

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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.

U2 - 10.4049/jimmunol.0902022

DO - 10.4049/jimmunol.0902022

M3 - Journal article

C2 - 19734208

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

ER -