Sjögren's disease & overlap diseases
Examining the biological pathways underlying clinical heterogeneity in Sjogren's syndrome: proteomic and network analysis
Authors' conclusion
Our data provide clues to the pathways contributing to the glandular and non-glandular manifestations of SS and to potential therapeutic targets for different SS subtypes.
Study context
- Population
- Sjogren's syndrome (SS) subjects stratified into four clinical subtypes by the Newcastle Sjogren's Stratification Tool (NSST)454 unique proteins · 5 O-link panels
- Participants
- 180 subjects
- Comparison
- Serum proteomic profiles across the four NSST clinical subtypes of SS
- Outcome
- Differential serum protein expression between SS subtypes
Methodological detailsproteomic and network analysis, ARACNE network reconstruction, reanalysis of phase III tocilizumab trial data stratified by NSST
- Proteomic and network analysis
- ARACNE network reconstruction
- Reanalysis of phase III tocilizumab trial data stratified by NSST
Main finding
As reported in the abstract
- Differential expression of chemokines, cytokines and the major autoantigen TRIM21 between the SS subtypes
- Differential expression of transcription factors associated with energy metabolism and redox balance: APE1/Ref-1, FOXO1, TIGAR and BACH1
- Differentially expressed proteins inter-related in network analysis, supporting distinct molecular networks underlying the clinical subtypes of SS
Further findings
Fatigue score in phase III tocilizumab trial, patients stratified at baseline by NSST
- Improvement of fatigue score only in the subtype expressing the highest levels of serum IL-6
Original publication
Examining the biological pathways underlying clinical heterogeneity in Sjogren's syndrome: proteomic and network analysis. Ann Rheum Dis. Published 2 January 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →