Interleukin‐10 receptor expression and signalling were down‐regulated in CD4 + T cells of lupus nephritis patients

Summary Studies have indicated that interleukin (IL)‐10 has a pathogenic role in systemic lupus erythematosus (SLE); however, a protective effect of IL‐10 in SLE was also observed. Because the exact mechanism of IL‐10 signalling in the pathogenesis of SLE is unclear, this study sought to assess the expression and signalling of interleukin‐10 receptor (IL‐10R) in peripheral leucocytes from patients with SLE. We used flow cytometry to examine the expression of IL‐10R1 on different peripheral leucocytes from 28 SLE patients, of whom 14 had lupus nephritis (LN) and 14 were healthy controls. We also examined the effects of IL‐10 on phosphorylation of signal transducer and activator of transcription (STAT)‐3 and STAT‐1 in peripheral blood mononuclear cells (PBMCs) obtained from 13 SLE patients and seven healthy controls. Plasma cytokines were detected by flow cytometric bead array (CBA) techniques. Although IL‐10R1 expression levels on each peripheral leucocyte subset from 28 SLE patients and 14 healthy controls were similar, the expression levels on CD4 + T cells from LN patients were significantly lower than on CD4 + T cells from controls and SLE patients without nephritis ( P  < 0·01). IL‐10R1 expression levels on CD4 + and CD8 + T cells were correlated negatively with the SLE disease activity index ( P  < 0·01). Additionally, the phosphorylation of STAT‐3 was delayed and reduced in PBMCs from LN patients and active SLE patients. Plasma IL‐10 levels were significantly higher in LN patients than controls. IL‐10R1 expression on CD4 + T cells and signalling in PBMCs were down‐regulated in LN patients, indicating that IL‐10 and its receptor may have a special role in LN pathogenesis.