TH1 cytokines as proatherogenic key players of atherosclerotic plaque progression

Dietel-Schor, B.; Furtmair, Roman; Urschel, Katharina; Tauchi, Miyuki; Achenbach, Sara J.

doi:10.1016/j.atherosclerosis.2020.10.102

Cited by 2 publications

(1 citation statement)

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“…Moreover, deficiency in a ubiquitin ligase, Peli1, causes hyperactivation of T cells and rendered T cells refractory to suppression by T regulatory cells and transforming growth factor (TGF)-β [27]. In line with this finding, we demonstrated in the present study that Peli1 is a critical factor in the maintenance of peripheral T-cell tolerance since we observed a pronounced increase of pro-atherogenic immune cells populations like Th1 subsets [28] and the proatherogenic Th17 and IL-17 producing cells [29] as well as Th2 cells and T follicular helper cells in Apoe −/− Peli1 −/− mice fed HCD. The frequency of T follicular helper subsets correlates positively with laboratory parameters of atherosclerosis progression suggesting the essential role of T follicular helper cells in promoting inflammatory response and atherosclerosis progression [30].…”

Section: Discussionsupporting

confidence: 84%

The E3 Ubiquitin Ligase Peli1 Deficiency Promotes Atherosclerosis Progression

Burger

Baptista

Roth

et al. 2022

Cells

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Background: Atherosclerosis is a chronic inflammatory vascular disease and the main cause of death and morbidity. Emerging evidence suggests that ubiquitination plays an important role in the pathogenesis of atherosclerosis including control of vascular inflammation, vascular smooth muscle cell (VSMC) function and atherosclerotic plaque stability. Peli1 a type of E3 ubiquitin ligase has emerged as a critical regulator of innate and adaptive immunity, however, its role in atherosclerosis remains to be elucidated. Methods: Apoe−/− mice and Peli1-deficient Apoe−/− Peli1−/− mice were subject to high cholesterol diet. Post sacrifice, serum was collected, and atherosclerotic plaque size and parameters of atherosclerotic plaque stability were evaluated. Immunoprofiling and foam cell quantification were performed. Results: Peli1 deficiency does not affect atherosclerosis lesion burden and cholesterol levels, but promotes VSMCs foam cells formation, necrotic core expansion, collagen, and fibrous cap reduction. Apoe−/− Peli1–/– mice exhibit a storm of inflammatory cytokines, expansion of Th1, Th1, Th17, and Tfh cells, a decrease in regulatory T and B cells and induction of pro-atherogenic serum level of IgG2a and IgE. Conclusions: In the present study, we uncover a crucial role for Peli1 in atherosclerosis as an important regulator of inflammation and VSMCs phenotypic modulation and subsequently atherosclerotic plaque destabilization.

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Section: Discussionsupporting

confidence: 84%