AI Article Synopsis
- T1/ST2 is a marker on type 2 helper cells, and this study explores its role in Leishmania infections in mice, particularly how a lack of ST2 may lead to a more beneficial T1 immune response.
- The researchers compared ST2 knockout mice to wild-type mice after infecting them with L. infantum, finding that the ST2 knockout mice were better at controlling the infection and had less organ enlargement.
- The results suggest that the absence of ST2 enhances protective immune responses, leading to increased levels of IFN-γ and reduced inflammatory markers, indicating a potential shift towards a T1 immune response.
Article Abstract
T1/ST2 is a surface marker selectively expressed on type 2 helper (T2) effector cells. As Leishmania infection in susceptible BALB/c mice have ascribed to a polarized T2 response, this study aim to investigate the T1/ST2 (the receptor for IL-33), as a typical T2 marker in the postulation that a shift towards a beneficial T1 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 T1 induction.
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| http://dx.doi.org/10.1016/j.actatropica.2017.04.011 | DOI Listing |
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