Artículos de revistas
Regulated expression of galectin-1 after in vitro productive infection with herpes simplex virus type 1: implications for T cell apoptosis
Fecha
2005-10Registro en:
Gonzalez, Maria Ines; Rubinstein, Natalia; Ilarregui, Juan Martin; Toscano, Marta Alicia; Sanjuan, Norberto Aníbal; et al.; Regulated expression of galectin-1 after in vitro productive infection with herpes simplex virus type 1: implications for T cell apoptosis; Biolife Sas; International Journal Of Immunopathology And Pharmacology; 18; 4; 10-2005; 615-623
0394-6320
2058-7384
CONICET Digital
CONICET
Autor
Gonzalez, Maria Ines
Rubinstein, Natalia
Ilarregui, Juan Martin
Toscano, Marta Alicia
Sanjuan, Norberto Aníbal
Rabinovich, Gabriel Adrián
Resumen
Apoptosis of cytotoxic T lymphocytes by herpes simplex virus type-1 (HSV-1) has been reported to be a relevant mechanism of viral immune evasion. Galectin-1 (Gal-1), an endogenous lectin involved in T-cell apoptosis, has recently gained considerable attention as a novel mechanism of tumor-immune evasion. Here we investigated whether infection of cells with HSV-1 can modulate the expression of Gal-1. Results show that pro-apoptotic Gal-1, but not Gal-3, is remarkably up-regulated in cell cultures infected with HSV-1. In addition, this protein is secreted to the extracellular milieu, where it contributes to apoptosis of activated T cells in a carbohydrate-dependent manner. Since many viruses have evolved mechanisms to counteract the antiviral response raised by the infected host, our results suggest that HSV-1 may use galectin-1 as a weapon to kill activated T cells and evade specific immune responses.