Congresos y reuniones científicas
Título:
PDL1-expressing B cells from mice infected with Trypanosoma cruzi suppress TNF production in vitro by a cell-contact mediated mechanism
Autor/es:
GOROSITO SERRAN, MELISA; TOSELLO BOARI, JIMENA; RAMELLO, MARIA CECILIA; FIOCCA VERNENGO, FACUNDO; BECCARIA, CRISTIAN G; MONTES, CAROLINA L; ACOSTA RODRIGUEZ E V; GRUPPI, ADRIANA
Reunión:
Congreso; IV LASID Meeting, LXIII Argentinean Immunology Society Meeting ? II French Argentinean Immunology Meeting-; 2015
Resumen:
Background: Our previous results showed that activated B cells and Plasma cells generated during Trypanosoma cruzi infection have high expression of the inhibitory molecule PD-L1. Methods and results: To evaluate the possible function of these cells in regulating effector immune responses, splenocytes from infected mice were depleted from B cells through magnetic negative selection and the non-B cell fraction (NonBF) obtained was cultured alone or with purified B cells (ratio 1:1) in the presence of T. cruzi antigens. The concentration of effector cytokines TNF, IFNg and IL10 were measured by ELISA in the culture supernatants. We found that the NonBF produced high levels of TNF after antigen stimulation, which decreased when B cells were added to the culture. No changes were observed in IFNg and IL10 concentrations. The inhibition of TNF production by B cells was reverted when the PD-1/PD-L1 pathway was blocked using an anti-PD-L1 antibody but not in the presence of the isotype control. Furthermore, we observed that B cells failed to inhibit TNF production by NonBF when cell-to-cell contact was blocked by a transwell system. Finally, by immunofluorescence we determined that plasma cells with high expression of PD-L1 coexpressed CD11c and were localized in extrafolicular focii of the spleen of infected mice, suggesting they are short-lived plasma cells. Conclusion: Our data indicate that B cells/plasma cells from T. cruzi infected mice could regulate TNF secretion through PD-L1 by a mechanism dependent on cell-to cell independent on cytokine-production.