Abstract
Abstract Foxp3+ regulatory T cells arise from precursors in the thymus and can be induced from naïve CD4 T cells. They are indispensable for maintaining self-tolerance and limiting collateral damage during an immune response. Under inflammatory conditions, Treg cells acquire plasticity and instability, ultimately leading to a loss of CD25 and FoxP3. These exTregs lose suppressive function. exTregs have been reported to express lineage-defining transcription factors of helper CD4 T cell like Th1, Th2, Th17 or Tfh cells. In mouse models of atherosclerosis, conversion of Tregs to exTregs is accelerated. The molecular mechanism of Tregs conversion to exTregs is unknown. Previous studies have shown that plasma IL-6 was increased in atherosclerosis. The IL6 receptor heterotrimer IL6R (CD126) and gp130 (CD130) is expressed in Treg cells. We hypothesized that IL-6 may play a role during the conversion of Treg to exTreg. Using Treg and exTreg cell lineage-tracker mice (FoxP3eGFP−Cre-ERT2 ROSA26CAG-fl-stop-fl-tdTomato) on the Apoe-/- background, we are able to distinguish Treg from exTreg that lost Foxp3 expression in mice model of atherosclerosis. We established an in vitro culture system for Treg cells based on bead-bound anti-CD3 and anti-CD28. Preliminary data showed that IL-6 dramatically increased the proportion of exTreg cells in vitro. These data suggest that IL-6 may promote Treg to exTreg conversion.
Published Version
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