HMGB1Modulates the Treg/Th17 Ratio in Atherosclerotic Patients

Abstract

The data in our study indicated that HMGB1 may promote atherosclerosis progression via modulating the imbalance in the Treg/Th17 ratio.

Glycyrrhizin, a High-Mobility Group Box 1 Inhibitor, Improves Lipid Metabolism and Suppresses Vascular Inflammation in Apolipoprotein E Knockout Mice

“…Inflammation has recently been recognized as a critical factor in and regulator of the initiation and progression of coronary heart diseases and eventually stroke; however, the mechanisms responsible for the development of microenvironmental disorders in atherosclerotic plaques caused by inflammatory responses have not yet been elucidated. HMGB1 is a pivotal inducer of macrophage activation [3], smooth muscle cell proliferation and migration [16], intercellular adhesion molecule (ICAM-1) and vascular cell adhesion molecule (VCAM-1) secretion by endothelial cells [17], and T lymphocyte proliferation and apoptosis [10] when exposed to cholesterol loads in human atherosclerotic lesions. HMGB1 also interacts with the receptor for advanced glycation end products or multiple TLRs and thus plays a role in inducing the release of cytokines, such as tumor necrosis factor (TNF)-a, IL-6, IL-1, and IL-8, to stimulate innate immunity.…”

“…Based on the findings of previous studies, including studies completed in our laboratory, we have determined that HMGB1 expression and Th17 cell percentages are increased, while Treg percentages are decreased in patients with unstable angina and non-ST-segment elevation myocardial infarction [9, 10]. Interestingly, HMGB1 levels were significantly correlated with imbalances in the Treg/Th17 ratio, suggesting that HMGB1 may be a new biomarker for the risk of cardiovascular death [10, 11].…”

“…Interestingly, HMGB1 levels were significantly correlated with imbalances in the Treg/Th17 ratio, suggesting that HMGB1 may be a new biomarker for the risk of cardiovascular death [10, 11]. However, whether selectively targeting HMGB1 can ameliorate atherosclerotic plaque progression has not been determined.…”

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

“…And then, cells were stimulated with 4μL/ mL phorbolmyristate acetate (PMA)/Ionomycin mixture (Lot LK-CS1001, Liankebio, China) for 6 h in the presence of 4μL/mL BFA/Monensin mixture (Lot LK-CS1002, Liankebio, China) [23].The proportions of cells CD4…”

“…+ RGC-32 + T cells was performed by flow cytometry using intracellular staining as previously described with minor modifications [23,24]. Briefly, Aliquots of heparinized whole blood (100 μL) and cultured PBMCs were surface labeled with antibodies of each subpopulation for 15 min at room temperature (RT).…”