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- W4313372023 abstract "Abstract The incidence of atherosclerosis is higher among patients with systemic lupus erythematosus (SLE). An imbalance between regulatory T cells (Treg) and follicular helper T cells (Tfh) occurs in the development and progression in both diseases. However, the mechanisms by which lupus T cells may aggravate atherosclerosis remain unclear. Pre-B-cell leukemia transcription factor 1 isoform d (Pbx1-d) is a lupus susceptibility gene and transgenic (Tg) Pbx1-d in CD4+ T cells expands Tfh and impairs Treg. Here, we investigated the role of CD4-Pbx1-d-Tg T cells in the low-density lipoprotein receptor-deficient (Ldlr−/−) mice, an experimental model for atherosclerosis. Pbx1-d T cells exacerbated atherosclerosis in Ldlr−/− mice as compared to B6 T cells. The enhanced atherosclerosis was associated with increased body weight, increased autoantibody production, reduced Treg in the aorta, as well as increased splenic Tfh frequency and impaired Treg cell suppressive markers. Dyslipidemia inhibited the differentiation and function of Treg cells in vitro. Moreover, Pbx1-d Treg cells were less suppressive than B6 control Treg cells in dyslipidemia conditions. Thus, our results showed that Pbx1-d-Tg T cells exacerbate atherosclerosis due to the dysregulated Treg and Tfh cells, briging autoimmunity and cardiovascular pathology." @default.
- W4313372023 created "2023-01-06" @default.
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- W4313372023 date "2020-05-01" @default.
- W4313372023 modified "2023-10-16" @default.
- W4313372023 title "Lupus susceptibility gene Pbx1 promotes atherosclerosis via dysfunctional T cells in a mouse model" @default.
- W4313372023 doi "https://doi.org/10.4049/jimmunol.204.supp.142.17" @default.
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