In this study, we investigated the effect of neutrophils stimulated with advanced glycated end products (AGEs), the marker of diabetes, on CD4+ T cell differentiation and its underlying mechanism. Our data showed that the cultural medium of healthy adult neutrophils treated with AGEs increased expressions of both Th1 (IFN- γ) and Th17 (IL-17) phenotypes and the transcription factors of Th1 (Tbet) and Th17 (ROR γt) in naive CD4+T cells and CD4+CD25+FoxP3+ (Treg) T cellsin vitro. Next, we found that AGEs induced the generations of myeloperoxidase (MPO) and neutrophil elastase (NE) in neutrophils; inhibition of MPO or NE attenuated the effect of AGE-stimulated neutrophils on CD4+ T cell bias. Furthermore, receptor for AGEs (RAGE) inhibitor interrupted AGE-induced MPO and NE expressions, but...
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