INDUCTION OF GALECTIN 1 EXPRESSION IN HIV-INFECTED CD4+ T CELLS MODULATES VIRAL REPLICATION.

RUBIONE, JULIA; DUETTE, GABRIEL; PEREYRA GERBER, PEHUEN ; GEFFNER, JORGE; MARIÑO, KARINA VALERIA; TOSCANO, MARTA A; RABINOVICH, GABRIEL A.; OSTROWSKI, MATÍAS

Mar del Plata

Congreso; SAIC/SAI/SAFE 2016; 2016

SAIC/SAI/SAFE

The sequential action of glycosyltransferases and glycosidases are responsible for modifying cell surface ́s glycans (cellular glycome). These changes can either expose or mask ligands for endogenous lectins, such as Galectins (Gal). Extracellular Gal-1 has important immunomodulatory functions by selectively delet- ing Th1 and Th17 cells and enabling the expansion of regulatory T cells. Herein, we show that in vitro infection of CD4+ T cells induces the expression and secretion of Gal-1. Moreover, HIV- infected cells exhibit an increased binding of extracellular Gal-1 to their surface suggesting that during HIV infection the cellular glycome is modi ed. We hypothesize that during HIV replication secreted Gal1 modulates the functionality of CD4+ T cell in an autocrinous manner. We successfully silenced Gal1 expression in primary CD4+ T cells and the model cell line, HeLa. We are cur- rently studying the contribution of this lectin to HIV replication and the immunomodulatory role of Gal1 in the context of HIV infection.