Journal
RHEUMATOLOGY
Volume 49, Issue 5, Pages 876-881Publisher
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/keq001
Keywords
Systemic lupus erythematosus; Innate immunity; Toll-like receptor; Toll-like receptor 7; Toll-like receptor 9; B cell; UNC93B1; Anti-dsDNA antibody; Autoimmune disease; Myeloid differentiation factor 88
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Funding
- Ministry of Education, Culture, Sports, Science and Technology, Japan
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Objectives. The transmembrane endoplasmic reticulum (ER) protein UNC93B plays an essential role in the normal response to signalling through intracellular Toll-like receptor (TLR) 3, TLR7, TLR8 and TLR9. In the current study, we examined the level of UNC93B expression on peripheral B cells from patients with active SLE, and investigated any correlation with SLE pathogenesis. Methods. Peripheral blood mononuclear cells (PBMCs) and B cells from 43 active SLE patients were analysed by quantitative RT-PCR to determine the precise levels of UNC93B mRNA. We also analysed UNC93B protein expression on B cells from SLE patients using immunoblotting. Results. The expression of UNC93B mRNA on PBMCs from active SLE patients was significantly higher than that of controls (P < 0.05). The intracellular expression level of UNC93B protein on CD20(+) B cells from active SLE patients was also higher than in the controls. Moreover, the expression of UNC93B on B cells from lupus patients correlated significantly with high titres of anti-dsDNA antibody (P < 0.05). Conclusions. Up-regulation of the ER membrane protein UNC93B on human lupus B cells suggests that TLR9 and UNC93B play a partial role in the pathogenesis of SLE by inducing defective peripheral B-cell tolerance.
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