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Regulation of CXCL16 expression and secretion by myeloid cells is not altered in rheumatoid arthritis
  1. Antoine WT van Lieshout (a.vanlieshout{at}reuma.umcn.nl)
  1. Radboud University Nijmegen Medical Centre, Netherlands
    1. Robbert van der Voort (r.vandervoort{at}chl.umcn.nl)
    1. Radboud University Nijmegen Medical Centre, Netherlands
      1. Liza WJ Toonen (l.toonen{at}ncmls.ru.nl)
      1. Radboud University Nijmegen Medical Centre, Netherlands
        1. Suzanne FG van Helden (s.vanhelden{at}ncmls.ru.nl)
        1. Radboud University Nijmegen Medical Centre, Netherlands
          1. Carl G Figdor (c.figdor{at}ncmls.ru.nl)
          1. Nijmegen Centre of Molecular Life Sciences, Netherlands
            1. Piet LCM van Riel (p.vanriel{at}reuma.umcn.nl)
            1. University Medical Center Nijmegen, Netherlands
              1. Timothy RDJ Radstake (t.radstake{at}reuma.umcn.nl)
              1. University Medical Center Nijmegen, Netherlands
                1. Gosse J Adema (g.adema{at}ncmls.ru.nl)
                1. Nijmegen Centre of Molecular Life Sciences, Netherlands

                  Abstract

                  Objective: The chemokine CXCL16 is secreted by macrophages and dendritic cells (DC) to attract memory type T cells. CXCL16 expression is increased in arthritic joints of patients with rheumatoid arthritis (RA) and a role for CXCL16 has been suggested in the pathogenesis of RA. To date, little is known about the regulation of CXCL16 on monocytes/macrophages and DC. The aim of this study was to elucidate how CXCL16 expression is regulated in healthy donors and patients with RA.

                  Methods: CD14+ cells were isolated from the peripheral blood or synovial fluid of RA patients and healthy controls, differentiated into different types of dendritic cells or macrophages and stimulated with various cytokines or LPS. Cell surface proteins, including surface CXCL16, were measured by flowcytometry and soluble CXCL16 was measured by ELISA.

                  Results: Distinct types of dendritic cells constitutively express and secrete CXCL16, which is not affected by maturation. Monocytes rapidly upregulate membrane-bound CXCL16 expression and release soluble CXCL16 upon culture. CXCL16 expression by monocytes is transiently inhibited by the TLR4 ligand LPS. Th2 type cytokines inhibit soluble CXCL16, whereas Th1 stimuli enhance its release. In RA monocytes/macrophages, neither CXCL16 expression, nor CXCL16 regulation is different from healthy controls.

                  Conclusions: Culture of monocytes is the main trigger for CXCL16 surface expression in vitro, which is not altered in RA. Together our data suggest that the increased CXCL16 expression in patients with RA is likely to be caused by increased influx of monocytes rather than intrinsic differences in CXCL16 regulation.

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