Regulation of Galectin-1 expression: new implications into feto-materno tolerance

R. RAMHORST, S, DURAND, N. RUBINSTEIN, M. TOSCANO, A. CORIGLIANO, S. GENTI AND G. RABINOVICH. DIVISION OF IMMUNOGENETICS, HTAL. DE CLÍNICAS “JOSÉ DE SAN MARTÍN”. FACULTAD DE MEDICINA UBA.

Hynes Convention Center, Boston MA, USA

Congreso; American Association of Immunology, Immunology 2006; 2006

The American Association of Immunologists

Trophoblastic cells have devised multiple strategies to evade maternal immune attack. To evaluate whether Gal-1 may play a role in the establishing feto-placental tolerance, we investigated Gal-1 expression in normal and pathological placental tissues. Western Blot analysis and immunohistochemistry revealed high expression of Gal-1 throughout all the gestation period. Moreover, moles have variable Gal-1 expression and JEG3, choriocarcinoma cells, expressed significantly high levels of this protein. Functional studies revealed that serum-free condition media (SFCM) obtained from JEG-3 cells, were able to suppress proliferation of polyclonally-activated PBMC (p<0,005; Student t test). This effect was enhanced when PBMC were further cultured with progesterone (p<0,005 Student t-test) and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. further cultured with progesterone (p<0,005 Student t-test) and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. Student t test). This effect was enhanced when PBMC were further cultured with progesterone (p<0,005 Student t-test) and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. further cultured with progesterone (p<0,005 Student t-test) and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. p<0,005; Student t test). This effect was enhanced when PBMC were further cultured with progesterone (p<0,005 Student t-test) and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. further cultured with progesterone (p<0,005 Student t-test) and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. t test). This effect was enhanced when PBMC were further cultured with progesterone (p<0,005 Student t-test) and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R. p<0,005 Student t-test) and partially prevented when anti-Gal-1 pAb was added to cell culture. The contribution of Gal-1 to the suppressive effect of JEG3 SFCM was confirmed by Annexin V staining, displaying a reduction in the apoptosis levels when activated PBMC were cultured in the presence of SFCM and anti-Gal-1 or inhibitory sugars. Moreover, when JEG3 cells and PBMC were co-cultured resembling fetomaternal interface, Gal-1 induces apoptosis of CD3+ T cells and this effect can be partially prevented by anti Gal-1 Ab. Here, we show that Gal-1 is differentially regulated throughout human gestation under physiological and pathological conditions strongly suggesting an important role in materno tolerance to fetal antigens. Supported by PIP 05-06 to R.R.