Glycobiology Advance Access published online on August 18, 2003
Glycobiology, doi:10.1093/glycob/cwg110
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© 2003 Oxford University Press
ORIGINAL ARTICLES
1 INSERM U526, labo virologie, Faculté de Médecine, Nice, France The massive T cell death that occurs in HIV type 1 (HIV-1) infection contributes profoundly to the pathophysiology associated with AIDS. The mechanisms controlling cell death of both infected and uninfected T cells (i.e., "bystander" death) are not completely understood. We have shown that HIV-1 infection of T cells results in altered glycosylation of cell surface glycoproteins; specifically it decreased sialylation and increased expression of core 2 O-glycans. Galectin-1 is an endogenous human lectin that recognizes these types of glycosylation changes and induces cell death of activated lymphocytes. Therefore we studied the possible contribution of galectin-1 in the pathophysiology of AIDS. O-glycans modifications were investigated on peripheral lymphocytes from AIDS patients. Oligosaccharides from CD43 and CD45 of CEM cells latently infected with HIV-1 were chemically analyzed. Consistent with our previous results, we show that HIV-1 infection results in accumulation of exposed lactosamine residues, oligosaccharides recognized by galectin-1 on cell surface glycoproteins. Both latently HIV-1 infected T cell lines and peripheral CD4 and CD8 T cells from AIDS patients exhibited exposed lactosamine residues, and demonstrated marked susceptibility to galectin-1-induced cell death, in contrast to control cultures or cells from uninfected donors. The fraction of cells that died in response to galectin-1 exceeded the fraction of infected cells, indicating that death of uninfected cells occurred. Altered cell surface glycosylation of T cells during HIV-1 infection increases the susceptibility to galectin-1-induced cell death, and this death pathway can contribute to loss of both infected and uninfected T cells in AIDS.
Revised on August 4, 2003
Accepted on August 5, 2003
Altered T cell surface glycosylation in HIV type 1 infection results in increased susceptibility to galectin-1-induced cell death
2 The Burnham Institute, La Jolla, California, USA
3 Service de Médecine Interne, Hôpital Archet 2, Nice, France
4 UCLA Department of Pathology and Laboratory Medicine, Los Angeles, California, USA
cell death, highly active antiretroviral therapy, T cells, core 2 O-glycan, lactosamine, poly-N-acetyllactosamine
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