REGULATED EXPRESSION OF GALECTIN-1 IN NORMAL AND PATHOLOGICAL PLACENTA: A POTENTIAL MECHANISM OF IMMUNE PRIVILEGE.

RAMHORST R; DURAND S; RUBINSTEIN N; TOSCANO M; CORIGLIANO A; GENTI S; RABINOVICH G

Córdoba, Argentina

Congreso; VII Latin American Congress of Immunology; 2005

Asociación Latinoamericana de Inmunología

Several apoptotic mechanisms contribute to the maintenance of feto-maternal tolerance, including TRAIL and Fas-FasL. To evaluate whether Gal-1 may play a  role in the establishing feto-maternal tolerance, we investigated Gal-1 expression in normal and pathological trophopastical tissues. Western blot analysis and immunohistochemistry of placental tissue revealed high expression of Gal-1 in the first trimester, which was modulated throughout gestation. Moreover, moles expressed Gal-1 at different levels and particularly JEG3 (a human choriocarcinoma cell line), expressed significantly higher levels of this protein. Functional studies revealed that conditioned media (CM) obtained from JEG3 cells were able to significantly suppress proliferation of polyclonally-activated PBMC (p<0.005; student t test). This effect was more pronounced when CM were obtained from JEG3 cells pretreated with progesterone (p<0.005; student t test). The contribution of Gal-1 to this effect was assessed by adding blocking antibodies and inhibitory sugars (TDG) to cell cultures and the effect also was evaluated by Annexin V staining. In this work we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions and might play a role in the generation of immune privilege at the human feto-maternal interface.