Unknown

Dataset Information

0

Apolipoprotein AI prevents regulatory to follicular helper T cell switching during atherosclerosis.


ABSTRACT: Regulatory T (Treg) cells contribute to the anti-inflammatory response during atherogenesis. Here we show that during atherogenesis Treg cells lose Foxp3 expression and their immunosuppressive function, leading to the conversion of a fraction of these cells into T follicular helper (Tfh) cells. We show that Tfh cells are pro-atherogenic and that their depletion reduces atherosclerosis. Mechanistically, the conversion of Treg cells to Tfh cells correlates with reduced expression of IL-2R? and pSTAT5 levels and increased expression of IL-6R?. In vitro, incubation of naive T cells with oxLDL prevents their differentiation into Treg cells. Furthermore, injection of lipid-free Apolipoprotein AI (ApoAI) into ApoE-/- mice reduces intracellular cholesterol levels in Treg cells and prevents their conversion into Tfh cells. Together our results suggest that ApoAI, the main protein in high-density lipoprotein particles, modulates the cellular fate of Treg cells and thus influences the immune response during atherosclerosis.

SUBMITTER: Gaddis DE 

PROVIDER: S-EPMC5854619 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

altmetric image

Publications


Regulatory T (Treg) cells contribute to the anti-inflammatory response during atherogenesis. Here we show that during atherogenesis Treg cells lose Foxp3 expression and their immunosuppressive function, leading to the conversion of a fraction of these cells into T follicular helper (Tfh) cells. We show that Tfh cells are pro-atherogenic and that their depletion reduces atherosclerosis. Mechanistically, the conversion of Treg cells to Tfh cells correlates with reduced expression of IL-2Rα and pST  ...[more]

Similar Datasets

| S-EPMC4975778 | biostudies-literature
| S-EPMC4191003 | biostudies-literature
| S-EPMC3428091 | biostudies-literature
| S-EPMC7181357 | biostudies-literature
| S-EPMC10202951 | biostudies-literature
| S-EPMC5413949 | biostudies-literature
| S-EPMC4309019 | biostudies-literature
| S-EPMC6465332 | biostudies-literature
| S-EPMC4616158 | biostudies-literature
| S-EPMC10978943 | biostudies-literature