title: Interleukin-10 receptor expression and signalling were down-regulated in CD4⁺ T cells of lupus nephritis patients.
abstract: 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.
authors.affiliation: Department of Rheumatology and Immunology, Shengjing Hospital, Shenyang, China.
authors.forename: H D
authors.initials: HD
authors.lastname: Cui
authors.forename: Z M
authors.initials: ZM
authors.lastname: Qi
authors.forename: L L
authors.initials: LL
authors.lastname: Yang
authors.forename: L
authors.initials: L
authors.lastname: Qi
authors.forename: N
authors.initials: N
authors.lastname: Zhang
authors.forename: X L
authors.initials: XL
authors.lastname: Zhang
authors.forename: S Y
authors.initials: SY
authors.lastname: Du
authors.forename: Y
authors.initials: Y
authors.lastname: Jiang
mesh_terms: D000293:Adolescent; D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002478:Cells, Cultured; D016207:Cytokines / Q000097:blood; D015536:Down-Regulation; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016753:Interleukin-10 / Q000097:blood*; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000235:genetics / Q000276:immunology; D008181:Lupus Nephritis / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010766:Phosphorylation; D053701:Receptors, Interleukin-10 / Q000235:genetics* / Q000378:metabolism*; D050794:STAT1 Transcription Factor / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D016207:Cytokines; D053701:Receptors, Interleukin-10; D050794:STAT1 Transcription Factor; C494079:STAT1 protein, human; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D016753:Interleukin-10