Xinhua Zhou1,2, Qingxiang Li2, Yun Li1, Jingjing Fu2, Feng Sun1, Yan Li3, Yushu Wang4, Yuan Jia1, Yanna Zhang5, Rulin Jia1, Fanlei Hu6,7,8, Yingni Li9. 1. Department of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), 11 Xizhimen South St, Beijing, 100044, China. 2. Clinical Laboratory, Third Hospital of Nanchang, Nanchang, 330009, China. 3. Clinical Laboratory, First People's Hospital of Jinzhong, Shanxi, 030600, China. 4. Inspection Center, Qindao University Medical College Affiliated Yantai Yuhuangding Hospital, Yantai, 264000, China. 5. Department of Endocrinology and Rheumatology, Rongcheng People's Hospital, Rongcheng, 264300, Shandong, China. 6. Department of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), 11 Xizhimen South St, Beijing, 100044, China. fanleihu@bjmu.edu.cn. 7. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, 100191, China. fanleihu@bjmu.edu.cn. 8. Department of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing, 100191, China. fanleihu@bjmu.edu.cn. 9. Department of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), 11 Xizhimen South St, Beijing, 100044, China. ying8436@aliyun.com.
Abstract
OBJECTIVE: To reveal the characteristics and potential role of natural killer T-like cells (NKT-like cells) in the pathogenesis of primary Sjögren's syndrome (pSS). METHODS: Forty-six patients with pSS and 30 healthy subjects were enrolled in the study. The frequencies and cell count of NKT-like cells as well as other lymphocyte subsets were analyzed by flow cytometry. The clinical and laboratory indicators of pSS patients were also collected. Then, the correlation between NKT-like cells and pSS patient manifestations was analyzed by Spearman's rank test. In addition, NKT-like cells before and after therapy were also compared. RESULTS: Both the number and the frequencies of NKT-like cells were significantly decreased in pSS patients. The counts of NKT-like cells were positively correlated with CD4+ T cells (r = 0.464, P = 0.001), CD8+ T cells (r = 0.363, P = 0.013), NK cells (r = 0.488, P = 0.001), and IgM levels (r = 0.443, P = 0.002), while negatively correlated with the disease duration (r = - 0.33, P = 0.027). Moreover, after effective therapy, NKT-like cells were recovered both in the cell counts and frequencies. CONCLUSION: In pSS, NKT-like cells were fundamentally decreased, potentially contributing to the disease pathogenesis. Modulating the status of NKT-like cells might provide a novel strategy for treating the disease. KEY POINTS: • NKT-like cells were significantly decreased in pSS patients. • NKT-like cells were correlated with pSS patient manifestations. • NKT-like cells might be serverd as a new marker for assessing the status of pSS.
OBJECTIVE: To reveal the characteristics and potential role of natural killer T-like cells (NKT-like cells) in the pathogenesis of primary Sjögren's syndrome (pSS). METHODS: Forty-six patients with pSS and 30 healthy subjects were enrolled in the study. The frequencies and cell count of NKT-like cells as well as other lymphocyte subsets were analyzed by flow cytometry. The clinical and laboratory indicators of pSS patients were also collected. Then, the correlation between NKT-like cells and pSS patient manifestations was analyzed by Spearman's rank test. In addition, NKT-like cells before and after therapy were also compared. RESULTS: Both the number and the frequencies of NKT-like cells were significantly decreased in pSS patients. The counts of NKT-like cells were positively correlated with CD4+ T cells (r = 0.464, P = 0.001), CD8+ T cells (r = 0.363, P = 0.013), NK cells (r = 0.488, P = 0.001), and IgM levels (r = 0.443, P = 0.002), while negatively correlated with the disease duration (r = - 0.33, P = 0.027). Moreover, after effective therapy, NKT-like cells were recovered both in the cell counts and frequencies. CONCLUSION: In pSS, NKT-like cells were fundamentally decreased, potentially contributing to the disease pathogenesis. Modulating the status of NKT-like cells might provide a novel strategy for treating the disease. KEY POINTS: • NKT-like cells were significantly decreased in pSS patients. • NKT-like cells were correlated with pSS patient manifestations. • NKT-like cells might be serverd as a new marker for assessing the status of pSS.