ReviewFrontiers in immunology2026
Pathogenesis of renal involvement in primary Sjögren's disease: convergence of multifactorial mechanisms on immune dysregulation.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary Sjögren's disease (pSjD) is a chronic systemic autoimmune disease in which immune-mediated pathology is not confined to exocrine glands but also affects multiple organ systems. Renal involvement constitutes a clinically meaningful manifestation of pSjD and may exert a considerable impact on disease progression, prognosis, and treatment selection. However, the pathogenic basis of renal injury in pSjD is still incompletely understood, and existing therapeutic approaches remain largely empirical. Available studies suggest that renal involvement in pSjD arises from the interaction of multiple determinants, including inherited susceptibility, environmental factors, and endocrine dysregulation. At the core of these pathogenic mechanisms lies persistent activation of the type I interferon (IFN-I) system and immune dysregulation driven by excessive responses of T and B lymphocytes. Such immune abnormalities favor sustained autoantibody production and ectopic germinal center (EGC) formation, thereby amplifying autoimmune inflammation and promoting renal structural and functional injury. Here, this review integrates relevant literature to examine the multifactorial pathogenic mechanisms described above and to systematically elucidate how these mechanisms drive autoimmune responses through diverse immune cell populations. In addition, the potential application prospects of relevant novel targeted therapeutic strategies in pSjD-related renal damage are discussed.
Indexed as
Identifiers
What OpenQuestion holds
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.