Affiliation:
1. Cincinnati Children’s Hospital Medical Center, OH (L.A., C.A.C.).
2. Division of Experimental Pathology, Department of Pathology and Laboratory Medicine, University of Cincinnati, OH (W.S.D.).
Abstract
Several studies in animal models and human cohorts have recently suggested that HDLs (high-density lipoproteins) not only modulate innate immune responses but also adaptative immune responses, particularly CD4+ T cells. CD4+ T cells are central effectors and regulators of the adaptive immune system, and any alterations in their homeostasis contribute to the pathogenesis of cardiovascular diseases, autoimmunity, and inflammatory diseases. In this review, we focus on how HDLs and their components affect CD4+ T-cell homeostasis by modulating cholesterol efflux, immune synapsis, proliferation, differentiation, oxidative stress, and apoptosis. While the effects of apoB-containing lipoproteins on T cells have been relatively well established, this review focuses specifically on new connections between HDL and CD4+ T cells. We present a model where HDL may modulate T cells through both direct and indirect mechanisms.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Cited by
1 articles.
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