CD39-positive Tregs increased during ECP treatment compared to HTxC. ECP-treated patients showed higher levels for T helper type 1 (Th1), Th2 and Th17 cytokines. Cytokine levels were higher in HTx patients with rejection before ECP treatment compared to patients Talazoparib supplier with prophylactic ECP treatment. We recommend a monitoring strategy that

includes the quantification and analysis of Tregs, pDCs and the immune balance status before and up to 12 months after starting ECP. “
“Galectin-9 (Gal-9) plays pivotal roles in the modulation of innate and adaptive immunity to suppress T-cell-mediated autoimmune models. However, it remains unclear if Gal-9 plays a suppressive role for T-cell function in non-autoimmune disease models. We assessed the effects of Gal-9 on experimental hypersensitivity pneumonitis induced by Trichosporon asahii. When Gal-9 was given subcutaneously to C57BL/6 mice at the time of challenge with T. asahii, it significantly suppressed T. asahii-induced lung inflammation, as the levels of IL-1, IL-6, IFN-γ, and IL-17 were significantly reduced in the BALF of Gal-9-treated mice. Moreover, co-culture of anti-CD3-stimulated CD4 T cells with BALF cells harvested from Gal-9-treated mice on day 1 resulted

in diminished CD4 T-cell proliferation and decreased levels of IFN-γ and IL-17. CD11b+Ly-6ChighF4/80+ HKI-272 mouse BALF Mϕ expanded by Gal-9 were responsible for the suppression. We further found in vitro that Gal-9, only in the presence of T. asahii, expands CD11b+Ly-6ChighF4/80+ cells from BM cells, and the cells suppress T-cell proliferation and IFN-γ and IL-17 production. The present results indicate that Gal-9 expands immunosuppressive CD11b+Ly-6Chigh Mϕ to ameliorate Th1/Th17 cell-mediated hypersensitivity pneumonitis. Galectin-9 (Gal-9), a β-galactoside binding lectin, is a ligand for T-cell immunoglobulin- and mucin domain-containing molecule 3 Amylase (Tim-3), which plays crucial roles in innate and adaptive immunity via Gal-9/Tim-3 interactions 1, 2. Tim-3 is expressed

on terminally differentiated Th1 cells, Th17 cells and innate immune cells, such as DC 2–4. Gal-9 induces apoptosis of activated Th1 and Th17 cells, in part, through the Ca2+-calpain-caspase1 pathway 5, resulting in the amelioration of immunopathology in murine autoimmune disease models such as collagen-induced arthritis (CIA), autoimmune diabetes, and EAE 2, 6, 7. Little is known, however, as to whether mechanisms other than apoptosis of Th1/Th17 cells are involved in Gal-9-mediated suppression of inflammation. We have shown, for example, that Gal-9 also enhances Treg generation from naïve CD4+ T cells in a murine CIA model 7. Although we have previously shown that Gal-9 induces DC maturation 8 and weakly promotes TNF-α production from DC 2, it has been widely accepted that certain types of Mϕ/DC, including myeloid-derived suppressor cells (MDSC) and regulatory DC (DCreg), also exhibit immunosuppressive function in a variety of immune responses 9–11.