B CELL RESPONSE IN TRYPANOSOMA CRUZI INFECTION IS IMPAIRED IN THE ABSENCE OF IL-17.

FIOCCA VERNENGO, FACUNDO; BECCARIA, CRISTIAN GABRIEL; GOROSITO SERRAN, MELISA; MONTES, CAROLINA L.; ACOSTA RODRIGUEZ EVA V; GRUPPI, ADRIANA

Mar del Plata

Congreso; LXIV Reunión científica anual de la Sociedad Argentina de Inmunología, en conjunto con la reunión anual de SAIC y SAFE; 2016

Sociedad Argentina de Inmunología, en conjunto con la reunión anual de SAIC y SAFE

311 (950) B CELL RESPONSE IN TRYPANOSOMA CRUZI INFECTION IS IMPAIRED IN THE ABSENCE OF IL-17. Facundo Fiocca Vernengo1, Cristian Gabriel Beccaría1, Me- lisa Gorosito Serrán1, Carolina Lucía Montes1, Eva Virginia Acosta Rodriguez1, Adriana Gruppi1.1CIBICI-CONICET . Departamento de Bioquímica Clínica e Inmunología, FCQ, UNC. Córdoba. Argentina.B cells and antibodies play a key role in pathogen clearance and host survival during extracellular parasite infections. The Germinal centers (GC) provide a microenvironment that stimulates and regulates the interactions of B cells with follicular Th (Tfh) cells, which provide the cognate help required for the generation of high af nity Ab-producing plasma cells and memory B cells. In the last years, IL-17 has been reported as a key cytokine that promote spontaneous GC formation and autoantibodies production. Our aim was to elucidate the role of IL-17 in the generation of B cell response in T. cruzi infection. For this purpose, IL-17A/F KO and C57BL/6 mice were infected with 15.000 trypomastigotes. We found that IL-17A/F KO were susceptible to infection (p=0,05) as they started dying at day 22-23 post infection (pi). Interestingly, IL-17A/F KO mice showed higher liver and spleen parasitism at day 24pi (p=0,0193 and 0,0006 respectively). By ow cytometry analysis we found that IL-17A/F KO mice had lower frequency (23dpi) and number (14 and 23dpi) of GC B cells than infected control mice (p= 0,0203, 0,0306 and 0,0186 respectively). In addition, B cell activation was affected in IL-17A/F KO mice as they showed higher frequency of naïve B cells. Notably, Bcl-6 expression on B cells was markedly affected on IL-17A/F KO mice. Surprisingly, plasma cell generation was similar in both experimental groups. At the opposite site, T fol- licular helper (Tfh) and T follicular regulatory (Tfr) cells frequencies were not markedly affected in IL-17A/F KO mice. However, Tfh cells generated in IL-17 de cient mice showed higher levels of the inhibi- tory molecule 2B4. Finally we found that IL17R expression on B cells was higher than on Tfh in C57BL/6 infected mice. In conclusion, IL-17 de ciency did not affect Tfh but was suf cient to evoke a defective B cell response, particularly impacting on B cells.