TY - JOUR T1 - Role of Fractalkine in the Pathogenesis of Primary Sjögren Syndrome: Increased Serum Levels of Fractalkine, Its Expression in Labial Salivary Glands, and the Association with Clinical Manifestations JF - The Journal of Rheumatology JO - J Rheumatol DO - 10.3899/jrheum.130892 SP - jrheum.130892 AU - Jae Ho Lee AU - Seung-Ki Kwok AU - Seung Min Jung AU - Jennifer Lee AU - Jae-Seon Lee AU - Seung Ye Baek AU - Eun-Kyung Kim AU - Ji Hyeon Ju AU - Sung-Hwan Park AU - Ho-Youn Kim Y1 - 2014/10/15 UR - http://www.jrheum.org/content/early/2014/10/08/jrheum.130892.abstract N2 - Objective To investigate the expression of fractalkine and identify the clinical effects of fractalkine and its receptor (CX3CR1) in patients with primary Sjögren syndrome (pSS). Methods Serum fractalkine levels were determined by ELISA. Immunohistochemical staining was done to compare the expression of fractalkine and CX3CR1 between salivary glands (SG) of patients with SS and controls. The cells to be merged with fractalkine were evaluated by confocal microscopy. Type of CX3CR1-expressing cells among infiltrating lymphocytes in SG was analyzed by confocal microscopy. Further, associations among fractalkine, proinflammatory cytokines, and clinical profiles were investigated. Results Serum fractalkine levels in patients with pSS were higher than those in the control group (p = 0.026). SG expression of fractalkine and its receptor was upregulated in patients with pSS compared to that in the controls by immunohistochemistry. Higher histological grade was associated with more fractalkine-positive cells per total epithelial cells. Epithelial cells were the main fractalkine-expressing cell type in the SG. Serum fractalkine levels were significantly correlated with proinflammatory cytokines levels (interleukin 17: r = 0.685, p = 0.029; tumor necrosis factor-α: r = 0.444, p = 0.003), antinuclear antibody (r = 0.349, p = 0.022), and immunoglobulin G levels (r = 0.325, p = 0.044). Serum fractalkine levels in patients with extraglandular manifestations of pSS were significantly higher than in those without extraglandular manifestations (p = 0.026). Conclusion Fractalkine and CX3CR1 may play a role in the pathogenesis of pSS, including extraglandular manifestations. ER -