CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
IL-6 MEDIATES GALECTIN-8 COSTIMULATORY ACTIVITY OF ANTIGEN-SPECIFIC CD4T CELL RESPONSE
Autor/es:
CECILIA ARAHÍ PRATO; OSCAR CAMPETELLA; JULIETA CARABELLI; MARIA DEL PILAR AOKI; LILIANA MARIA SANMARCO; MARIA VIRGINIA TRIBULATTI
Lugar:
Buenos Aires
Reunión:
Congreso; I Reunión de Biociencias; 2017
Institución organizadora:
Sociedad Argentina de Protozoologia
Resumen:
Galectin-8 (Gal-8) is a mammalian lectin endowed with the ability to co-stimulate the antigen-specifc immune response. IL-6is a pleiotropic cytokine that plays an important role in the regulation of antigen-specifc T cell response. In the present study, weaimed to elucidate whether IL-6 was mediating Gal-8 costimulatory effect on antigen-specifc CD4T cells. Firstly, we quantifed IL-6by ELISA in supernatants from DO11.10TCROVA mouse splenocytecultures, stimulated with the cognate peptide OVA (OVA), Gal-8 orthe combination of both. Notably, IL-6 was signifcantly increasedin the conditioned media from Gal-8- or Gal-8 plus OVA-treatedcells but not from OVA only-treated cells, where IL-6 was presentat the same level as in untreated cells. Next, to assess if IL-6 isinvolved in Gal-8 costimulatory effect, splenocytes were stimulated,as before, but in the presence of an IL-6-neutralizing monoclonalantibody or a matching isotype control, and T cell proliferation was determined. Interestingly, IL-6 neutralization specifcally precludedGal-8 costimulatory activity but did not affect antigen-specifc T cellresponse. To identify those cells that produce IL-6 in response toGal-8, intracellular IL-6 was determined by FACS in Gal-8-stimulated BALB/cJ splenocytes. We found that both CD11c+ and CD11b+cells produced IL-6 in response to Gal-8. Finally, to confrm that IL-6from antigen-presenting cells was mediating the Gal-8 costimulatoryeffect, splenocytes from IL-6-defcient (IL6KO) or C57BL/6J (wildtype) mice pre-treated with Mitomycin-C, were co-cultured with purifed CD4T cells from OTII mice in the presence of OVA, Gal-8 orthe combination of both. In agreement, Gal-8-induced costimulationof antigen-specifc CD4T cell response was signifcantly impairedwhen APC from IL-6KO mice were used. Taken together, our resultsargue in favor of the participation of IL-6 in the immunostimulatorypathway induced by Gal-8.