Publications
Find coverage of the latest original articles on Lupus, focusing on those with data on therapeutic interventions and those that have clinical impact.
April 2024
Type I interferon blockade with anifrolumab in patients with systemic lupus erythematosus modulates key immunopathological pathways in a gene expression and proteomic analysis of two Phase 3 trials
Ann Rheum Dis 2024 DOI 10.1136/ard-2023-225445 Epub ahead of print https://pubmed.ncbi.nlm.nih.gov/38569851/
Type I IFN blockade with anifrolumab modulated multiple inflammatory pathways downstream of type I IFN signalling.
January 2024
Burden of Systemic Lupus Erythematosus in Clinical Practice: Baseline Data from the SLE Prospective Observational Cohort Study (SPOCS) by Interferon Gene Signature
Lupus Sci Med. 2023; 10(2):e001032 DOI: 10.1136/lupus-2023-001032
This study from Arnaud et al described baseline characteristics of SLE patients grouped by disease activity and IFNGS category in the international SPOCS study. IFNGS-high patients were younger at SLE diagnosis, and a baseline SLEDAI-2K score ≥10 was associated with shorter disease duration, more frequent and more severe flares. IFNGS-low patients were more likely to exhibit musculoskeletal and CNS comorbidities than IFNGS-high patients. Continuation of the SPOCS study will allow investigation into how different baseline characteristics affect long-term outcomes in SLE patients.
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March 2023
2022 EULAR points to consider for the measurement, reporting and application of IFN-I pathway activation assays in clinical research and practice
Ann Rheum Dis. 2023 doi: 10.1136/ard-2022-223628
The first EULAR-endorsed points to consider (PtC) for the measurement and reporting of IFN-I assays in clinical research and practice are developed.
May 2022
High Systemic Type I Interferon Activity Is Associated with Active Class III/IV Lupus Nephritis
The Journal of Rheumatology 2022; 49:388–97 DOI 10.3899/jrheum.210391
Iwamoto, et al. aimed to determine the association of serum IFN activity with subtypes of lupus nephritis. This study suggests that systemic high type I IFN in SLE is involved in the pathogenesis of severe class III/IV LN and contributes to severe kidney involvement in European-American patients with SLE. However, this effect was independent of anti‑dsDNA antibody status and complement levels. Expression of type I IFN was not found to be clearly related to plasmacytoid dendritic cell infiltration, although it did directly stimulate podocytes to induce chemokines and molecules related to podocyte injury.