Abstract
Vaccination with the respiratory syncytial virus (RSV) attachment (G) protein results in immune-mediated lung injury after natural RSV infection with pathogenic features characteristic of an exaggerated Th2 response. Here we demonstrate that approximately half of the CD4(+) T cells infiltrating the lungs of G-primed mice utilize a single V beta gene (V beta 14) with remarkably limited CDR3 diversity. Furthermore, elimination of these V beta 14-bearing CD4(+) T cells in vivo abolishes the type 2-like pulmonary injury. These results suggest that a novel subset of CD4(+) T cells may be crucial in the development of pathology during human RSV infection and that genetic or environmental factors prior to or at the time of G antigen exposure may affect the commitment of this discrete antigen-specific T cell subset to Th2 differentiation.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antigens, Viral / immunology*
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CD4-Positive T-Lymphocytes / immunology*
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Cells, Cultured
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Complementarity Determining Regions / genetics
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Female
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Immunoglobulin Variable Region / genetics
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Immunologic Memory
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Lung / immunology
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Lymphocyte Activation
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Lymphocyte Depletion
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Mice
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Mice, Inbred BALB C
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Pulmonary Eosinophilia / immunology
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Receptors, Antigen, T-Cell, alpha-beta / genetics
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Respiratory Syncytial Virus Infections / immunology*
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Respiratory Syncytial Virus Infections / pathology
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Respiratory Syncytial Viruses / immunology
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T-Lymphocyte Subsets / classification
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Th2 Cells / immunology
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Viral Proteins / immunology*
Substances
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Antigens, Viral
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Complementarity Determining Regions
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Immunoglobulin Variable Region
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Receptors, Antigen, T-Cell, alpha-beta
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Viral Proteins