Aberrant Distribution of CD3+CD56+ NKT-like Cells in Patients with Primary Sjögren's Syndrome.

Objective To elucidate the potential role of CD3(+)CD56(+) NKT-like cells in the pathogenesis of primary Sjogren's syndrome (pSS). Methods 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 inununohis to chemistry, respectively. The chemotaxis of NKT-like cells was examined by transwell migration assay. Results Peripheral NKT-like cells from pSS patients were significantly lower than those from HC (3.09 +/- 235% vs. 537 +/- 4.06%, p=0.0002), which was negatively correlated with European League Against Rheumatism Sjogren'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-alpha and IFN-gamma, which was promoted by CX3CL1 in vitro. Conclusion 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 he implicated in the pathogenesis of pSS.