RT Journal Article
SR Electronic
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
FD The Journal of Rheumatology
SP 2425
OP 2438
DO 10.3899/jrheum.130892
VO 41
IS 12
A1 Jae Ho Lee
A1 Seung-Ki Kwok
A1 Seung Min Jung
A1 Jennifer Lee
A1 Jae-Seon Lee
A1 Seung Ye Baek
A1 Eun-Kyung Kim
A1 Ji Hyeon Ju
A1 Sung-Hwan Park
A1 Ho-Youn Kim
YR 2014
UL http://www.jrheum.org/content/41/12/2425.abstract
AB 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.