Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Journal of Immunology |
| Vol/bind | 176 |
| Udgave nummer | 7 |
| Sider (fra-til) | 4235-43 |
| Antal sider | 8 |
| ISSN | 0022-1767 |
| Status | Udgivet - 2006 |
Bibliografisk note
Keywords: Animals; CD8-Positive T-Lymphocytes; Chemokine CXCL10; Chemokine CXCL11; Chemokine CXCL9; Chemokines, CXC; Gene Expression Regulation, Viral; Immunologic Surveillance; Kinetics; Ligands; Lymphocytic Choriomeningitis; Lymphocytic choriomeningitis virus; Meningitis, Viral; Mice; Mice, Knockout; Receptors, CXCR3; Receptors, ChemokineCitationsformater
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CXCL10 is the key ligand for CXCR3 on CD8+ effector T cells involved in immune surveillance of the lymphocytic choriomeningitis virus-infected central nervous system. / Christensen, Jeanette Erbo; de Lemos, Carina; Moos, Torben; Christensen, Jan Pravsgaard; Thomsen, Allan Randrup.
I: Journal of Immunology, Bind 176, Nr. 7, 2006, s. 4235-43.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - CXCL10 is the key ligand for CXCR3 on CD8+ effector T cells involved in immune surveillance of the lymphocytic choriomeningitis virus-infected central nervous system
AU - Christensen, Jeanette Erbo
AU - de Lemos, Carina
AU - Moos, Torben
AU - Christensen, Jan Pravsgaard
AU - Thomsen, Allan Randrup
N1 - Keywords: Animals; CD8-Positive T-Lymphocytes; Chemokine CXCL10; Chemokine CXCL11; Chemokine CXCL9; Chemokines, CXC; Gene Expression Regulation, Viral; Immunologic Surveillance; Kinetics; Ligands; Lymphocytic Choriomeningitis; Lymphocytic choriomeningitis virus; Meningitis, Viral; Mice; Mice, Knockout; Receptors, CXCR3; Receptors, Chemokine
PY - 2006
Y1 - 2006
N2 - IFN-gamma-inducible protein 10/CXCL10 is a chemokine associated with type 1 T cell responses, regulating the migration of activated T cells through binding to the CXCR3 receptor. Expression of both CXCL10 and CXCR3 are observed during immunopathological diseases of the CNS, and this receptor/ligand pair is thought to play a central role in regulating T cell-mediated inflammation in this organ site. In this report, we investigated the role of CXCL10 in regulating CD8(+) T cell-mediated inflammation in the virus-infected brain. This was done through analysis of CXCL10-deficient mice infected intracerebrally with lymphocytic choriomeningitis virus, which in normal immunocompetent mice induces a fatal CD8(+) T cell-mediated meningoencephalitis. We found that a normal antiviral CD8(+) T cell response was generated in CXCL10-deficient mice, and that lack of CXCL10 had no influence on the accumulation of mononuclear cells in the cerebrospinal fluid. However, analysis of the susceptibility of CXCL10-deficient mice to lymphocytic choriomeningitis virus-induced meningitis revealed that these mice just like CXCR3-deficient mice were partially resistant to this disease, whereas wild-type mice invariably died. Furthermore, despite marked up-regulation of the two remaining CXCR3 ligands: CXCL9 and 11, we found a reduced accumulation of CD8(+) T cells in the brain parenchyma around the time point when wild-type mice succumb as a result of CD8(+) T cell-mediated inflammation. Thus, taken together these results indicate a central role for CXCL10 in regulating the accumulation of effector T cells at sites of CNS inflammation, with no apparent compensatory effect of other CXCR3 ligands.
AB - IFN-gamma-inducible protein 10/CXCL10 is a chemokine associated with type 1 T cell responses, regulating the migration of activated T cells through binding to the CXCR3 receptor. Expression of both CXCL10 and CXCR3 are observed during immunopathological diseases of the CNS, and this receptor/ligand pair is thought to play a central role in regulating T cell-mediated inflammation in this organ site. In this report, we investigated the role of CXCL10 in regulating CD8(+) T cell-mediated inflammation in the virus-infected brain. This was done through analysis of CXCL10-deficient mice infected intracerebrally with lymphocytic choriomeningitis virus, which in normal immunocompetent mice induces a fatal CD8(+) T cell-mediated meningoencephalitis. We found that a normal antiviral CD8(+) T cell response was generated in CXCL10-deficient mice, and that lack of CXCL10 had no influence on the accumulation of mononuclear cells in the cerebrospinal fluid. However, analysis of the susceptibility of CXCL10-deficient mice to lymphocytic choriomeningitis virus-induced meningitis revealed that these mice just like CXCR3-deficient mice were partially resistant to this disease, whereas wild-type mice invariably died. Furthermore, despite marked up-regulation of the two remaining CXCR3 ligands: CXCL9 and 11, we found a reduced accumulation of CD8(+) T cells in the brain parenchyma around the time point when wild-type mice succumb as a result of CD8(+) T cell-mediated inflammation. Thus, taken together these results indicate a central role for CXCL10 in regulating the accumulation of effector T cells at sites of CNS inflammation, with no apparent compensatory effect of other CXCR3 ligands.
M3 - Journal article
C2 - 16547260
VL - 176
SP - 4235
EP - 4243
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 7
ER -