ArticleRheumatology and immunology research2025
Investigating the role of tripartite motif containing-21 and interleukin-6 in pro-Inflammatory symptom-associated heterogeneity within primary Sjögren's syndrome.
Article in Rheumatology and immunology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background and Objectives: In Primary Sjögren's Syndrome (pSS) clinical heterogeneity is a challenge to both treatment and disease understanding. Variations in symptoms may be driven by different underlying biological pathways. Tripartite motif containing-21 (TRIM21) and interleukin-6 (IL-6) have been implicated in autoimmunity and inflammation, with links to chronic interferon activity. We assess the levels of TRIM21 and IL-6 in the context of anti-Ro autoantibody status, and in different symptom-based pSS subgroups we have previously described, to explore whether they may contribute to the clinical heterogeneity in pSS. Methods: We measured serum IL-6 concentrations for 193 pSS patients and 18 healthy controls, and analysed available microarray data for TRIM21 transcript expression in 184 pSS patients and 33 healthy controls. Levels of IL-6 and TRIM21 were analysed in the context of symptom-based subgroups, anti-Ro autoantibody status and symptom scores. Results: TRIM21 and IL-6 levels were significantly raised in pSS patients compared to healthy controls. TRIM21 expression was similar between symptom-based subgroups, whilst IL-6 concentrations were significantly increased in the high symptom burden group compared to the low symptom burden group. TRIM21 levels were significantly increased in Ro+ autoantibody groups compared to Ro-, whilst IL-6 levels were similar between groups. Conclusions: Our results suggest a potential role for IL-6 in the pathogenesis of the high symptom burden group. Increased TRIM21 transcript levels in the Ro+ group supports the hypothesis of suggests autoantibody targeting of the TRIM21 protein leading to aberrant type I interferon (IFN) production which in turn may drive further TRIM21 transcript production.
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