Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing; Key Laboratory of Rheumatology & Clinical Immunology, Ministry of Education, Beijing; and Department of Rheumatology and Clinical Immunology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing, China.
Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing; Key Laboratory of Rheumatology & Clinical Immunology, Ministry of Education, Beijing; and Department of Rheumatology and Clinical Immunology, South Campus, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Clin Exp Rheumatol. 2021 Jan-Feb;39(1):98-104. doi: 10.55563/clinexprheumatol/uzzz6d. Epub 2020 Apr 3.
To elucidate the potential role of CD3+CD56+ NKT-like cells in the pathogenesis of primary Sjögren's syndrome (pSS).
We enrolled pSS patients and healthy controls and examined the peripheral population, the surface chemokine receptors and the proinflammatory cytokine production of NKT-like cells by flow cytometry. The infiltration of NKT-like cells in the labial salivary gland (LSG) was examined by immunofluorescence. Serum and tissue levels of CX3CL1 were detected by Cytometric Bead Array and immunohistochemistry, respectively. The chemotaxis of NKT-like cells was examined by transwell migration assay.
Peripheral NKT-like cells from pSS patients were significantly lower than those from HC (3.09±2.35% vs. 5.37±4.06%, p=0.0002), which was negatively correlated with European League Against Rheumatism Sjögren's Syndrome Disease Activity index. NKT-like cells infiltrated into the LSG of pSS patients. Serum and LSG epithelial CX3CL1 levels were higher in pSS patients than those in HC, which promoted the chemotaxis of the NKT-like cells. NKT-like cells from pSS patients expressed a higher level of CD69, and secreted high level of TNF-α and IFN-γ, which was promoted by CX3CL1 in vitro.
NKT-like cells decreased in peripheral and infiltrated into the LSG of the pSS patients, which could be driven by CX3CL1-CX3CR1 axis. NKT-like cells might be implicated in the pathogenesis of pSS.
阐明 CD3+CD56+NKT 样细胞在原发性干燥综合征（pSS）发病机制中的潜在作用。
我们招募了 pSS 患者和健康对照者，通过流式细胞术检测 NKT 样细胞的外周群体、表面趋化因子受体和促炎细胞因子产生情况。通过免疫荧光法检测唇腺（LSG）中 NKT 样细胞的浸润情况。通过 Cytometric Bead Array 和免疫组化法分别检测血清和组织中 CX3CL1 的水平。通过 Transwell 迁移实验检测 NKT 样细胞的趋化性。
pSS 患者外周血 NKT 样细胞明显低于 HC（3.09±2.35% vs. 5.37±4.06%，p=0.0002），与欧洲抗风湿病联盟干燥综合征疾病活动指数呈负相关。NKT 样细胞浸润到 pSS 患者的 LSG 中。pSS 患者血清和 LSG 上皮细胞 CX3CL1 水平高于 HC，促进了 NKT 样细胞的趋化性。pSS 患者的 NKT 样细胞表达更高水平的 CD69，并分泌高水平的 TNF-α和 IFN-γ，这在体外可被 CX3CL1 促进。
pSS 患者外周血和 LSG 中的 NKT 样细胞减少，可能由 CX3CL1-CX3CR1 轴驱动。NKT 样细胞可能与 pSS 的发病机制有关。
