Galectin-1 confers immune privilege to human trophoblast: implications in recurrent fetal loss

RAMHORST R.E.; GIRIBALDI L.; FRACCAROLI L.; TOSCANO M.A.; STUPIRSKI J.C.; ROMERO M.D.; DURAND E.S.; RUBINSTEIN N.; BLASCHITZ A.; SEDLMAYR P.; GENTI-RAIMONDI S.; FAINBOIM L.; RABINOVICH G.A.

OXFORD UNIV PRESS INC

Lugar: Oxford; Año: 2012 vol. 22 p. 1374 - 1374

echanisms accounting for the protection of the fetal semi-allograft from maternal immune cells remain incompletely understood. In previous studies, we showed that galectin-1 (Gal1), an immunoregulatory glycan-binding protein, hierarchically triggers a cascade of tolerogenic events at the mouse fetomaternal interface. Here, we show that Gal1 confers immune privilege to human trophoblast cells through the modulation of a number of regulatory mechanisms. Gal1 was mainly expressed in invasive extravillous trophoblast cells of human first trimester and term placenta in direct contact with maternal tissue. Expression of Gal1 by the human trophoblast cell line JEG-3 was primarily controlled by progesterone and pro-inflammatory cytokines and impaired T-cell responses by limiting T cell viability, suppressing the secretion of Th1-type cytokines and favoring the expansion of CD4(+)CD25(+)FoxP3(+) regulatory T (T(reg)) cells. Targeted inhibition of Gal1 expression through antibody (Ab)-mediated