ReviewJournal of clinical medicine2026
Update on the Aetiopathogenesis of Sjögren Disease: From Interferon Signaling to Epithelial Dysfunction.
Review in Journal of clinical medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- [How often do patients with Sjögren's syndrome fulfil the activity criteria for immunomodulatory treatment?]Zeitschrift fur Rheumatologie · 2026Article
- Inflammasomes in Sjögren's Disease: Exploring the Therapeutic Value.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sjögren disease (SjD) is a prototypical autoimmune disease whose management has long suffered from a limited understanding of its underlying pathophysiological mechanisms. However, major advances have been made over the past decade. The innate immune system is now recognized as playing a key role in the early stages of the disease, particularly through activation of interferon (IFN) pathways, driven in part by epithelial cells, which actively attract autoreactive lymphocytes. Furthermore, the mechanisms of B-cell activation in SjD are now better understood, notably with the recognition of BAFF (B-cell activating factor), a Tumor necrosis factor (TNF) family cytokine, whose production is highly dependent on type I and II IFN signaling. The involvement of other cell types, such as fibroblasts and T cells, has also been underlined. Significant progress has been achieved in elucidating lymphomagenesis, the most severe complication of SjD. Together, these advances provide a clearer picture of SjD pathogenesis and open avenues for the development of new targeted therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.