摘要：SummaryGlucose, the critical energy source in the human body, is considered a potential risk factor in various autoimmune diseases when consumed in high amounts. However, the roles of glucose at moderate doses in the regulation of autoimmune inflammatory diseases and CD4+T cell responses are controversial. Here, we show that while glucose at a high concentration (20% w/v) promotes intestinal inflammation, it suppresses colitis at a moderate dose (6% w/v), which increases the proportion of intestinal regulatory T (Treg) cells but does not affect effector CD4+T cells. Glucose treatment promotes Treg cell differentiation but it does not affect Treg stability. Feeding glucose alters gut microbiota compositions, which are not involved in the glucose induction of Treg cells. Glucose promotes aryl hydrocarbon receptor (AhR) activation to induce Treg polarization. These findings reveal the different effects of glucose at different doses on the intestinal immune response.Graphical abstractDisplay OmittedHighlights•A moderate dose of glucose suppresses intestinal inflammation•Glucose promotes Treg differentiation but not Treg stability•Microbiota are not involved in the glucose induction of Treg cells•AhR mediates the glucose induction of Treg cellsBiological sciences; Immunology; Components of the immune system; Cell biology
