IL17RA regulates the magnitude of CD8+ T cell response to T. cruzi by modulating apoptosis, cell exhaustion and memory differentiation

JIMENA TOSELLO BOARI; FACUNDO FIOCCA-VERNENGO; CECILIA RAMELLO; CAROLINA AMEZCUA-VESELY; CINTIA ARAUJO-FURLAN; MELISA GOROSITO SERRAN; CAROLINA MONTES; ADRIANA GRUPPI; EVA V ACOSTA-RODRIGUEZ

Congreso; LXI Reunión Anual de la Sociedad Argentina de Inmunología; 2013

Sociedad Argentina de Inmunología

IL-17RA-signaling promotes host survival during T. cruzi infection by controlling exacerbated inflammation, but additional protective mechanisms would be involved. As development of robust CD8+ T cell (CTL) immunity is a key element for host resistance to T. cruzi, we aimed at evaluating if IL17RA is involved in the generation of protective CTL responses. To address this, we evaluated the magnitude and quality of the CTL response in infected IL17RA knockout (INF-KO) mice in comparison to WT controls. INF-KO mice showed increased tissue parasitism in spleen and liver that correlated with reduced numbers of CTL specific for the inmunodominant T. cruzi epitope TSKB20 (TSKB20-specific CTL, spleen, d20pi: 1,7±1,4x106 in KO vs 5,5±2,3x106 in WT mice, p