Regulated expression of galectin-1 after in vitro productive infection with herpes simplex virus type 1: implications for T cell apoptosis.
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.
Gonzalez
M I
MI
Department of Microbiology, School of Medicine, University of Buenos Aires, Argentina.
Rubinstein
N
N
Ilarregui
J M
JM
Toscano
M A
MA
Sanjuan
N A
NA
Rabinovich
G A
GA
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015153:Blotting, Western; D002522:Chlorocebus aethiops; D004591:Electrophoresis, Polyacrylamide Gel; D004847:Epithelial Cells / Q000473:pathology; D019084:Fluorescent Antibody Technique, Indirect; D037483:Galectin 1 / Q000096:biosynthesis* / Q000235:genetics; D037502:Galectin 3 / Q000235:genetics / Q000502:physiology; D005786:Gene Expression Regulation / Q000502:physiology*; D006561:Herpes Simplex / Q000473:pathology*; D018259:Herpesvirus 1, Human; D006801:Humans; D007108:Immune Tolerance; D013601:T-Lymphocytes / Q000473:pathology*; D014709:Vero Cells
D037483:Galectin 1; D037502:Galectin 3