Glycodelin A and galectin-1: Role in foetal tolerance

Foetal immunotolerance is one of the major challenges of pregnancy which is surmounted in part by both, the foetus and the mother. This review highlights the role of two decidual proteins, galectin-1 and glycodelin A (GdA) in achieving localized immunosuppressive state in the uterus. The two proteins have similar effects on T cells, inhibiting their proliferation, inducing apoptosis, inhibiting IL-2 production, but, helping in the expansion of Treg cells. They also induce tolerogenicity in dendritic cells, B cells and monocytes. In addition, GdA suppresses the lytic activity of cytotoxic T cells and induces apoptosis in monocytes as well as NK cells. Overall, galectin-1 and GdA inhibit the proliferation of immune cells, decrease their cytotoxicity and induce an anti-inflammatory cytokine environment. Thus leading to modulation of the immune response at the feto-maternal interface aiding in the maintenance of pregnancy to full term. The two proteins, other than having overlapping functions share similarity only in being lectins. Both are structurally different; galectin-1 has a non-glycosylated β-sandwich while GdA has a glycosylated β-barrel. Evolutionarily, GdA is found only in higher primates and appears to be functionally restricted to pregnancy, whereas galectin-1 is found in most mammals and has a role in immunomodulation at almost all immune privileged sites.