Journal
IMMUNITY
Volume 15, Issue 4, Pages 637-646Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(01)00209-6
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Funding
- NHLBI NIH HHS [HL-10446] Funding Source: Medline
- NIAID NIH HHS [AI-17672, AI-37293, AI-34607] Funding Source: Medline
- NIAMS NIH HHS [AR-35506] Funding Source: Medline
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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 VP 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.
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