LECTIN-INDUCED IMMUNOREGULATION IN OVINE PLACENTA

MERCEDES IGLESIAS*; GABRIEL RABINOVICH*; CLAUDIA SOTOMAYOR; CARLOTA WOLFENSTEIN-TODEL

Electronic Lectin Journal: Lectins, Biology, Biochemistry and Clinical Biochemistry

Thorkilds, Denmark

Lugar: http://plab.ku.dk/tcbh/Lectins12/Iglesias/paper.htm; Año: 1998 vol. 12 p. 94 - 110

0723-8878

A paradox about pregnancy is that the placenta, a semi-allograft of fetal tissue, avoids maternal immune rejection (1). Its importance is underscored by its location in the maternal-fetal interface, and it appears to act as a protection shield for the fetus. Fetal trophoblasts use several mechanisms to subvert normal maternal immune response. These include: a) selective expression of immune antigens critical to alloreactivity, such as expression of HLA-G by cytotrophoblasts, b) impaired responses to immune-activating cytokines present in placental tissue and c) secretion of factors which may suppress local immune responsiveness (2). Evidently, there is a bidirectional interaction between the maternal immune system and the feto-placental unit during pregnancy, with the placenta acting, not only as a sieve or a transport system, but also as an important source of immunomodulatory substances, such as Th2-cytokines (3-4), TGF- (5) and hormones (6). Recently, several carbohydrate-binding proteins have been isolated from ovine placenta in our laboratory. These include a 14 kDa type (galectin-1) (7), a 29 kDa type (galectin-3) (8), a sialic acid-binding lectin (9) and a heparin-binding lectin (10). Since many cell growth regulatory and immunomodulatory functions have been attributed to galectins (11-16), it was particularly attractive to explore the immunological properties of these coexisting ovine placental lectins. In the present study we provide evidence that galectins-1 and -3 copurified from placental tissue at mid-gestation, exert antagonic inhibitory and stimulatory effects. Furthermore the sialic acid-binding lectin induced a decrease of lymphocyte proliferative response, while the heparin-binding lectin did not induce any significant change on cell growth.