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Modulation of CD8+ T cell avidity by increasing the turnover of viral antigen during infection.
Gray, Peter M; Parks, Griffith D; Alexander-Miller, Martha A.
Afiliación
  • Gray PM; Department of Microbiology and Immunology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
Cell Immunol ; 231(1-2): 14-9, 2004.
Article en En | MEDLINE | ID: mdl-15919365
The increased potency of high avidity CD8+ T cells for the clearance of viral infections has been well documented. We have previously reported the novel finding that intranasal infection with the paramyxovirus SV5 induces a CD8+ T cell response to the SV5 P protein that is almost exclusively of high avidity. Based on our results that the level of peptide presentation is a critical factor in the selective expansion of high versus low avidity cells in vitro, we hypothesized that the avidity of the anti-viral response generated in vivo could be altered by increasing the turnover of the P protein during viral infection through linkage to ubiquitin (UbP). Infection with a virus expressing UbP (VV-UbP) elicited a significant increase in low avidity cells in both BALB/c and C3H mice compared to the almost exclusively high avidity response elicited by VV-P. Our results are the first demonstration of the control of avidity during the antiviral response through an engineered change to a viral antigen. The implications of our findings for vaccine development are discussed.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T CD8-positivos / Infecciones por Rubulavirus / Virus de la Parainfluenza 5 / Antígenos Virales Límite: Animals Idioma: En Revista: Cell Immunol Año: 2004 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos
Buscar en Google
Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T CD8-positivos / Infecciones por Rubulavirus / Virus de la Parainfluenza 5 / Antígenos Virales Límite: Animals Idioma: En Revista: Cell Immunol Año: 2004 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos