作者: Hsin-Yuan Cheng , Dalia E. Gaddis , Runpei Wu , Chantel McSkimming , LaTeira D. Haynes
DOI: 10.1172/JCI83136
关键词: Cellular differentiation 、 Downregulation and upregulation 、 LDL receptor 、 Regulatory T cell differentiation 、 Cell growth 、 T cell differentiation 、 Biology 、 Internal medicine 、 Endocrinology 、 PI3K/AKT/mTOR pathway 、 T cell
摘要: ATP-binding cassette transporter G1 (ABCG1) promotes cholesterol accumulation and alters T cell homeostasis, which may contribute to progression of atherosclerosis. Here, we investigated how the selective loss ABCG1 in cells impacts atherosclerosis LDL receptor-deficient (LDLR-deficient) mice, a model disease. In LDLR-deficient mice fed high-cholesterol diet, cell-specific deficiency protected against atherosclerotic lesions. Furthermore, led 30% increase Treg percentages aorta aorta-draining lymph nodes (LNs) these compared with animals only LDLR deficiency. When Abcg1 was selectively deleted Tregs observed LNs reduced absence ABCG1, intracellular downregulation mTOR pathway, increased differentiation naive CD4 into Tregs. The resulted activation IL-10 production by cells. Last, found that higher expression associated frequency human blood samples. Our study indicates regulates Tregs, highlighting pathway can influence homeostasis