SynthesisFrontiers in immunology2026
Familial and genetic overlap between Sjögren's disease and other autoimmune diseases.
Synthesis in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Inflammasomes in Sjögren's Disease: Exploring the Therapeutic Value.International journal of molecular sciences · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To evaluate familial clustering of Sjögren's disease (SjD) with other autoimmune diseases and to characterize shared genetic architecture using an integrative genomic approach. Methods: Meta-analysis identified studies assessing autoimmune disease incidence in probands and first-degree relatives (FDRs), and pooled relative risks (RRs) were calculated. Publicly available genome-wide association study (GWAS) summary statistics were analyzed within a hierarchical genetic architecture framework integrating genome-wide polygenic correlation (LDSC), locus-level overlap (Jaccard index), union-based susceptibility mapping, and SNP-level pleiotropy detection. Results: Eighteen studies evaluated familial aggregation of SjD and other autoimmune diseases, of which nine were included in the pooled analysis. The RR of SjD was 10.54 when both proband and FDR were affected. Among discordant autoimmune probands, systemic lupus erythematosus (SLE) showed the highest RR for SjD (4.49), followed by systemic sclerosis (2.65). Genome-wide analyses demonstrated substantial polygenic sharing between SjD and systemic autoimmune diseases, positioning SjD as a bridging disorder. However, locus-level overlap was largely driven by the HLA region; after HLA exclusion, shared loci markedly decreased and were restricted to a limited number of immune regulatory hubs. SNP-level pleiotropy analyses similarly indicated predominantly HLA-dependent sharing with fewer non-HLA signals. Conclusion: SjD shows strong familial aggregation and shared genetic susceptibility with multiple autoimmune diseases. These findings support a hierarchical model in which broad HLA-driven polygenic sharing coexists with selective non-HLA convergence. Strengths and limitations of this study: This study integrates systematic familial meta-analysis with GWAS data to characterize shared autoimmune genetic architecture. However, inference regarding shared causal variants remains limited by reliance on summary statistics and locus-based resolution.
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