Author:
Gaddis Dalia E.,Wu Runpei,Parks John S.,Sorci-Thomas Mary G.,Hedrick Catherine C.
Abstract
ABSTRACTApolipoprotein A1 (ApoA1), the major constituent of the high-density lipoprotein (HDL) molecule, exhibits anti-inflammatory properties. Our laboratory has previously shown that ApoA1 protects against switching of regulatory T (Treg) cells to atherogenic T follicular helper cells in Western diet-fed mice. However, the role of ApoA1 in modulating Treg cell homeostasis in the absence of atherosclerosis remains uncharacterized. Here, we show that ApoA1 is required for normal Treg cell homeostasis and functioning at steady state. Specifically, lack of ApoA1 decreased the numbers of both natural and induced Treg cells and also lowered Treg cell-based homeostatic proliferation and suppressive functions. Importantly, these changes occurred without affecting other T cell populations. Finally, we determined that the observed phenotypes were caused by changes to cholesterol content and reduced interleukin-2 (IL-2) receptor signaling in ApoA1-deficient Treg cells. Overall, our results show that ApoA1-HDL is necessary for Treg cell homeostasis and functioning.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献