Zhaoliang Su1, Hongxiang Lu2, Haiqiang Jiang3, Haitao Zhu2, Ze Li4, Pan Zhang2, Ping Ni2, Huiling Shen5, Wenlin Xu5, Huaxi Xu6. 1. The Central Laboratory, the Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China; Department of Immunology, School of Medicine, Jiangsu University, Zhenjiang, 212013, China. 2. Department of Immunology, School of Medicine, Jiangsu University, Zhenjiang, 212013, China. 3. Department of Immunology, School of Medicine, Jiangsu University, Zhenjiang, 212013, China; Department of Laboratory Medicine, The Affiliated Jiangyin Hospital of Nanjing University of Chinese Medicine, Jiangyin, 214400, China. 4. Department of Cardiology, The Fourth Hospital of Shanxi, Xi'an, 710043, China. 5. The Central Laboratory, the Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China. 6. The Central Laboratory, the Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China. Electronic address: szl30@yeah.net.
Abstract
BACKGROUND: IFN-γ-producing Th17 cells have been implicated in autoimmune disorders, but their properties in humans are known only partially. The molecular mechanisms and external factors that govern IFN-γ-producing Th17-cell bias are incompletely understood. The present work was to clarify whether (i) IFN-γ-producing Th17 cells are present in the peripheral circulation of patients with coronary atherosclerosis (CA); (ii) high mobility group box (HMGB)1 in circulation is associated with IFN-γ-producing Th17-cell bias. METHODS: Thirty-six patients (17 females and 19 males; 45-84 years) diagnosed as having atherosclerosis after coronary angiography for suspected or known CA were included the study cohort. Samples of peripheral blood were collected from healthy volunteers and patients, and classical tests (flow cytometry, RT-qPCR) were used to measure blood components. RESULTS AND CONCLUSION: Our results clearly demonstrated that HMGB1 were up-regulated in different progressive CA patients: 5.38 ± 1.48 ng/ml, 6.30 ± 1.53 ng/ml and 5.86 ± 1.12 ng/ml vs1.45 ± 0.65 ng/ml for only atherosclerotic plaque (AP), atherosclerotic plaque and some plaque rupture, no thrombosis (PR), plaque rupture and accompanying thrombosis (TH) and volunteers, respectively, p < 0.05. The frequency of IFN-γ-producing Th17 cells was 2.33 ± 0.58%, 1.93 ± 0.2% and 2.21 ± 0.65% vs 0.38 ± 0.21% for AP, PR, TH and volunteers, p < 0.05, respectively. Furthermore, HMGB1 contributed to IFN-γ-producing Th17-cell bias by controlling expression of T-bet and RUNX3. We demonstrated, for the first time, that HMGB1 is a potential inducer of IFN-γ-producing Th17-cell bias, and that IFN-γ-producing Th17 cells might be one of the pathogenic factors in atherosclerosis.
BACKGROUND: IFN-γ-producing Th17 cells have been implicated in autoimmune disorders, but their properties in humans are known only partially. The molecular mechanisms and external factors that govern IFN-γ-producing Th17-cell bias are incompletely understood. The present work was to clarify whether (i) IFN-γ-producing Th17 cells are present in the peripheral circulation of patients with coronary atherosclerosis (CA); (ii) high mobility group box (HMGB)1 in circulation is associated with IFN-γ-producing Th17-cell bias. METHODS: Thirty-six patients (17 females and 19 males; 45-84 years) diagnosed as having atherosclerosis after coronary angiography for suspected or known CA were included the study cohort. Samples of peripheral blood were collected from healthy volunteers and patients, and classical tests (flow cytometry, RT-qPCR) were used to measure blood components. RESULTS AND CONCLUSION: Our results clearly demonstrated that HMGB1 were up-regulated in different progressive CA patients: 5.38 ± 1.48 ng/ml, 6.30 ± 1.53 ng/ml and 5.86 ± 1.12 ng/ml vs1.45 ± 0.65 ng/ml for only atherosclerotic plaque (AP), atherosclerotic plaque and some plaque rupture, no thrombosis (PR), plaque rupture and accompanying thrombosis (TH) and volunteers, respectively, p < 0.05. The frequency of IFN-γ-producing Th17 cells was 2.33 ± 0.58%, 1.93 ± 0.2% and 2.21 ± 0.65% vs 0.38 ± 0.21% for AP, PR, TH and volunteers, p < 0.05, respectively. Furthermore, HMGB1 contributed to IFN-γ-producing Th17-cell bias by controlling expression of T-bet and RUNX3. We demonstrated, for the first time, that HMGB1 is a potential inducer of IFN-γ-producing Th17-cell bias, and that IFN-γ-producing Th17 cells might be one of the pathogenic factors in atherosclerosis.
Authors: Qinjie Zhou; Diego F Niño; Yukihiro Yamaguchi; Sanxia Wang; William B Fulton; Hongpeng Jia; Peng Lu; Thomas Prindle; David Pamies; Meaghan Morris; Liam L Chen; Chhinder P Sodhi; David J Hackam Journal: Sci Transl Med Date: 2021-01-06 Impact factor: 17.956
Authors: Bernardo L Rapoport; Helen C Steel; Annette J Theron; Liezl Heyman; Teresa Smit; Yastira Ramdas; Ronald Anderson Journal: Cells Date: 2020-07-10 Impact factor: 6.600
Authors: Liangjie Xu; Tianxin Geng; Guangyao Zang; Li Bo; Yi Liang; Hong Zhou; Jinchuan Yan Journal: J Cell Mol Med Date: 2020-03-09 Impact factor: 5.310