机构：[1]Guangzhou University of Chinese Medicine, Guangzhou, People’s Republicof China[2]The First Affiliated Hospital of Guangzhou University of ChineseMedicine, The Lingnan Medicine Research Center, Guangzhou 510405,People’s Republic of China[3]Department of Laboratory Medicine,Guangdong Second Provincial General Hospital, Guangzhou 510317, People’sRepublic of China[4]Department of Hematology Oncology, GuangzhouMedical University, Guangzhou Women and Children’s Medical Center,Guangzhou 510623, People’s Republic of China
Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease. The dysregulated immune system plays an important role in the pathogenesis of AS. Myeloid-derived suppressor cells (MDSCs) play a key immunoregulatory role in autoimmune arthritis. The aim of this study was to clarify the underlying immunoregulatory mechanism of MDSCs in patients with AS.
Flow cytometry was used to analyze the phenotype of MDSCs among peripheral blood mononuclear cells (PBMCs) from 46 patients with AS and 46 healthy control subjects. The correlation between MDSC frequency and the disease index of patients with AS was evaluated. A T cell proliferation experiment was used to evaluate the immunosuppressive function of MDSCs.
Polymorphonuclear (PMN) and monocytic (M)-MDSCs were significantly elevated in the PBMCs of patients with AS, when compared with levels in healthy controls. Additionally, M-MDSC levels correlated positively with the clinical index of AS, including the Bath ankylosing spondylitis disease activity index (BASDAI) score, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels. M-MDSCs derived from patients with AS suppressed T cell responses, and this effect was dependent on the induction of arginase-I. Furthermore, AS-derived M-MDSCs showed high levels of phosphorylated STAT3. Stattic, a STAT3-specific inhibitor, and STAT3-targeted siRNA abrogated the immunosuppressive function of M-MDSCs. Inhibition of STAT3 signaling also resulted in decreased arginase-I activity.
STAT3/arginase-I signaling plays an important role in both the expansion and activation of M-MDSCs in patients with AS. This information may be beneficial in developing novel therapeutic strategies for preventing AS.
基金：
the National Natural Science Foundation of
China (81700512) to YL; Natural Science Foundation of Guangdong Province
(2016A030310252) to YL; Guandong Second Provincial General Hospital
Youth Fund (YQ2016-007) to ZL
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2017]版：
大类|2 区医学
小类|2 区风湿病学
最新[2025]版：
大类|2 区医学
小类|2 区风湿病学
第一作者：
第一作者机构：[1]Guangzhou University of Chinese Medicine, Guangzhou, People’s Republicof China[2]The First Affiliated Hospital of Guangzhou University of ChineseMedicine, The Lingnan Medicine Research Center, Guangzhou 510405,People’s Republic of China
通讯作者：
通讯机构：[1]Guangzhou University of Chinese Medicine, Guangzhou, People’s Republicof China[2]The First Affiliated Hospital of Guangzhou University of ChineseMedicine, The Lingnan Medicine Research Center, Guangzhou 510405,People’s Republic of China
推荐引用方式(GB/T 7714)：
Liu Yu-Feng,Zhuang Kun-Hai,Chen Bin,et al.Expansion and activation of monocytic-myeloid-derived suppressor cell via STAT3/arginase-I signaling in patients with ankylosing spondylitis.[J].Arthritis research & therapy.2018,20(1):168.doi:10.1186/s13075-018-1654-4.
APA：
Liu Yu-Feng,Zhuang Kun-Hai,Chen Bin,Li Pei-Wu,Zhou Xuan...&Liu Feng-Bin.(2018).Expansion and activation of monocytic-myeloid-derived suppressor cell via STAT3/arginase-I signaling in patients with ankylosing spondylitis..Arthritis research & therapy,20,(1)
MLA：
Liu Yu-Feng,et al."Expansion and activation of monocytic-myeloid-derived suppressor cell via STAT3/arginase-I signaling in patients with ankylosing spondylitis.".Arthritis research & therapy 20..1(2018):168
医学