Journal
FRONTIERS IN IMMUNOLOGY
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2020.622326
Keywords
C-reactive protein; type I interferons; systemic lupus erythematosus; inflammation; biomarker; pentraxins; interferon; gene variants
Categories
Funding
- Swedish Research Council for Medicine and Health
- Swedish Society of Medicine
- Swedish Rheumatism Association
- Region Ostergotland (ALF grants)
- King Gustaf V's 80-year Anniversary Foundation
- King Gustaf V and Queen Victoria's Freemasons' Foundation
- Gustafsson Foundation
- Selander Foundation
- Alfred Osterlund Foundation
- Anna-Greta Crafoord Foundation
- Greta and Johan Kock's Foundation
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In patients with systemic lupus erythematosus (SLE) during a quiescent phase, IL-6 levels, CRP genotype (rs1205), and type I interferon (IFN) gene signature have an impact on basal CRP levels, with IL-6 positively associated and IGS positivity and CRP genotype (rs1205) AA/GA negatively associated with CRP levels.
Objectives Patients with systemic lupus erythematosus (SLE) often display modest elevations of C-reactive protein (CRP) despite raised disease activity and increased interleukin (IL-) 6. We asked to what extent IL-6 levels, the CRP polymorphism rs1205, and the type I interferon (IFN) gene signature affects the basal CRP levels in patients with SLE during a quiescent phase of the disease. Methods CRP and IL-6 were analyzed in plasma from 57 patients meeting established classification criteria for SLE. The CRP polymorphism rs1205 was assessed and gene expression analyzed including four type I IFN-regulated genes (IGS). Results CRP was increased in patients with detectable IL-6 levels (p=0.001) and decreased among IGS-positive subjects (p=0.033). A multiple linear regression model revealed IL-6 to have a positive association with CRP levels, whereas both IGS-positivity and CRP genotype (rs1205) AA/GA were negatively associated with CRP-levels. Conclusion Our data offer an explanation to the modest CRP levels seen in viral infections and IFN-alpha driven autoimmunity and corroborate prior observations showing an IFN-alpha dependent downregulation of CRP. The latter observation, together with the fact that the CRP-lowering polymorphism rs1205 is overrepresented in human SLE, could explain low basal CRP and inadequate CRP-responses among patients with active SLE.
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