Background
This study aimed to investigate the mechanism of galectin (Gal)-1 of regulating Treg/Th17 in pathogenesis of acute rejection after liver transplantation in rat.
Conclusions
In aggregate, Gal-1 promotes Treg differentiation in CD4+ T cells though NF-κB/RelB-IL-27 pathway. These findings suggest a new therapeutic target to mediate Treg population.
Methods
Mononuclear cells were induced to immature dendritic cells (imDCs), which were transfected with or without NF-κB/RelB. Western Blot was performed to detect the expression of NF-κB/RelB. the expression of CD11c, CD45RB, CD80 and MHC II were detected by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was employed to detect cytokines IL-27 and TGF-β. Lewis and dark agouti (DA) rats were generally anaesthetized by isoflurane inhalation to establish liver transplant models.
Results
We demonstrate that Gal-1 disturbs maturation of imDCs by downregulating NF-κB/RelB expression, and Gal-1 negatively controls CD4+ proliferation though IL-27 pathway. Conclusions: In aggregate, Gal-1 promotes Treg differentiation in CD4+ T cells though NF-κB/RelB-IL-27 pathway. These findings suggest a new therapeutic target to mediate Treg population.