T1/ST2 deficient mice display protection against Leishmania infantum experimental infection

Abstract

T1/ST2 is a surface marker selectively expressed on type 2 helper (TH2) effector cells. As Leishmania infection in susceptible BALB/c mice have ascribed to a polarized TH2 response, this study aim to investigate the T1/ST2 (the receptor for IL-33), as a typical TH2 marker in the postulation that a shift towards a beneficial TH1 response would occur in the absence of ST2. For this, ST2 knockout (ST2−/−) and WT BALB/c mice were experimentally infected in the retro-orbital sinus with L. infantum. We showed that ST2−/− animals displayed better control of parasite burden in both spleen and liver tissues at different time points of chronic phases, and reduced spleenomegaly and hepatomegaly compared with the wild-type (WT) mice. This was associated with increased in the IFN-γ levels and expression by CD4+ and CD8+ lymphocytes. The inflammatory response encompasses transaminases (AST and ALT) releases and NO productions were remarkably lower in ST2−/− mice compared with WT. These data suggest that, ST2−/−) exert protection against L. infantum infection and probably shift the immune response toward TH1 induction.