Abstract |
Interactions between fractalkine (CX3CL1) and its receptor, CX3CR1, mediate leukocyte adhesion, activation, and trafficking. The respiratory syncytial virus (RSV) G protein has a CX3C chemokine motif that can bind CX3CR1 and modify CXCL1-mediated responses. In this study, we show that expression of the RSV G protein or the G protein CX3C motif during infection is associated with reduced CX3CR1+ T cell trafficking to the lung, reduced frequencies of RSV-specific, MHC class I-restricted IFN-gamma-expressing cells, and lower numbers of IL-4- and CX3CL1-expressing cells. In addition, we show that CX3CR1+ cells constitute a major component of the cytotoxic response to RSV infection. These results suggest that G protein and the G protein CX3C motif reduce the antiviral T cell response to RSV infection.
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Authors | Jennifer Harcourt, Rene Alvarez, Les P Jones, Christine Henderson, Larry J Anderson, Ralph A Tripp |
Journal | Journal of immunology (Baltimore, Md. : 1950)
(J Immunol)
Vol. 176
Issue 3
Pg. 1600-8
(Feb 01 2006)
ISSN: 0022-1767 [Print] United States |
PMID | 16424189
(Publication Type: Journal Article)
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Chemical References |
- CX3C Chemokine Receptor 1
- Chemokines, CX3C
- Cx3cr1 protein, mouse
- Receptors, Chemokine
- Viral Envelope Proteins
- attachment protein G
- Interleukin-4
- Interferon-gamma
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Topics |
- Amino Acid Motifs
- Animals
- CD4-Positive T-Lymphocytes
(immunology, metabolism)
- CD8-Positive T-Lymphocytes
(metabolism)
- CX3C Chemokine Receptor 1
- Cell Migration Inhibition
- Cell Movement
(immunology)
- Cells, Cultured
- Chemokines, CX3C
(biosynthesis, genetics)
- Female
- Interferon-gamma
(biosynthesis, genetics)
- Interleukin-4
(metabolism)
- Lung
(immunology, pathology)
- Mice
- Mice, Inbred BALB C
- Receptors, Chemokine
(antagonists & inhibitors, biosynthesis)
- Respiratory Syncytial Viruses
(genetics, immunology)
- T-Lymphocytes
(immunology, metabolism, pathology, virology)
- Viral Envelope Proteins
(biosynthesis, genetics, immunology)
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