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Enhanced interleukin-10 production by dendritic cells upon stimulation with Toll-like receptor 4 agonists in systemic sclerosis that is possibly implicated in CCL18 secretion
Scandinavian Journal of Rheumatology , 03/06/09

van Lieshout AWT et al. - Elevated CCL18 levels in systemic sclerosis (SSc) are not caused by an intrinsically enhanced CCL18 secretion by monocytes/macrophages but are, at least partly, orchestrated by an enhanced IL-10 secretion by Toll-like receptor 4 (TLR4)-stimulated dendritic cells (DCs), suggesting a role for TLR4 ligands and DCs in the pathogenesis of SSc.

Methods

Study to determine whether TLR-mediated stimulation of monocytes and DCs contributes to the higher levels of CCL18 in SSc
CCL18 levels measured in 40 SSc pts, pts with primary Raynaud's phenomenon (RP) and healthy controls
Presence of TLR4 agonists in the circulation of SSc pts was investigated using TLR4 transgenic CHO cells
CCL18 and IL-10 secretion by monocytes/macrophages and monocyte-derived DCs (moDCs) measured in the supernatant
Indirect effect of lipopolysaccharide (LPS)-stimulated moDCs on CCL18 secretion by monocytes/macrophages investigated using a transwell system

Results

CCL18 levels were elevated in SSc pts vs pts with RP and healthy controls
SSc sera strongly induced CD25 expression on CHO cells expressing TLR4 vs SLE pts or controls
Neither monocytes/macrophages nor moDCs from SSc pts secreted higher levels of CCL18
However, moDCs matured with the TLR4 ligand LPS from pts with SSc secreted higher amounts of IL-10

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