Regulation of CXCL16 expression and secretion by myeloid cells is not altered in rheumatoid arthritis.
Publication year
2009Source
Annals of the Rheumatic Diseases, 68, 6, (2009), pp. 1036-43ISSN
Publication type
Article / Letter to editor

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Organization
Rheumatology
CHL
Laboratory of Hematology
Tumorimmunology
Journal title
Annals of the Rheumatic Diseases
Volume
vol. 68
Issue
iss. 6
Page start
p. 1036
Page end
p. 43
Subject
N4i 4: Auto-immunity, transplantation and immunotherapy; NCMLS 1: Infection and autoimmunity; NCMLS 2: Immune Regulation; ONCOL 3: Translational researchAbstract
OBJECTIVE: Chemokine (C-X-C motif) ligand 16 (CXCL16) is secreted by macrophages and dendritic cells (DCs) 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 DCs. 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 patients with RA and healthy controls, differentiated into different types of dendritic cells or macrophages and stimulated with various cytokines or lipopolysaccharide (LPS). Cell surface proteins, including surface CXCL16, were measured by flow cytometry 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 Toll-like receptor (TLR)4 ligand LPS. Th2 type cytokines inhibit soluble CXCL16, whereas T helper (Th)1 cell stimulus enhances 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.
This item appears in the following Collection(s)
- Academic publications [227693]
- Faculty of Medical Sciences [86198]
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