INVESTIGADORES
MOTRAN Claudia Cristina
congresos y reuniones científicas
Título:
“Modulation of antigen specific immune response by pregnancy specific glycoprotein 1a (PSG1a)-treated dendritic cells”.
Autor/es:
MOTRAN, CLAUDIA C; MONTES, CAROLINA L; MARTINEZ, FERNANDO; LOPEZ DIAZ, FERNANDO; BOCCO, JOSE L; GRUPPI, ADRIANA
Lugar:
CORDOBA
Reunión:
Congreso; VII Congreso Latinoamericano de Inmunologia; 2005
Institución organizadora:
ASOCIACION LATINOAMERICANA DE INMUNOLOGIA
Resumen:
MODULATION OF ANTIGEN SPECIFIC IMMUNE RESPONSE BY PREGNANCY SPECIFIC GLYCOPROTEIN 1a (PSG1a)-TREATED DENDRITIC CELLS. Motran, C., Montes, C., Martínez, F., López Díaz, F., Bocco, J.L. and Gruppi, A. CIBICI. Córdoba. ARGENTINA. We demonstrated that PSG1a, the major PSG isoform released to maternal circulation during the pregnancy, is able to modulate the cellular immune response acting through antigen presenting cells (APCs). Considering that dendritic cells (DCs) are uniquely able to initiate responses in naïve T cells and also participates in T helper cell (Th) education, the aim of this study was to determine whether PSG1a is able to modulate the DC metabolism and APC function to regulate T cell response. For that, DC were cultured 18 h with medium alone, PSG1a (culture supernatant of Vaccinia-PSG1a-infected J774 cells) or control supernatant (culture supernatant of Vaccinia wt-J774 infected cells) and the activity of arginase and iNOS enzymes were evaluated. In addition, we studied by FACS the expression of MHCII, CD80 and CD86 and evaluated the ability of these cells to induce OVA-specific T cell response in vivo. We observed that rec-PSG1a is able to up-regulate arginase activity and MHCII expression and down regulate CD80 expression over the control while no differences between the groups were observed for iNOS activity and CD86 expression.  In addition, ex vivo treatment of OVA-pulsed DC with PSG1a impairs the ability of these cells to induce OVA-specific T cell proliferation as well as Th1 and Th2 cytokine secretion when injected in mice. Our results suggest that the treatment with PSG1a could be exploited as a novel approach for down-regulate unwanted T cell response.