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Lookup NU author(s): Lauren Scott, Dr Joe Berry, Dr Kyle Thompson, Dr Jessica Tarn, Karl Wood, John CasementORCiD, Professor Fai NgORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2025 Lauren R Scott, Joe Berry, Kyle Thompson, Jessica Tarn, Karl Wood, John Casement, Wan-Fai Ng, published by De Gruyter on behalf of NCRC-DID.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.
Author(s): Scott LR, Berry J, Thompson K, Tarn J, Wood K, Casement J, Ng W-F
Publication type: Article
Publication status: Published
Journal: Rheumatology and Immunology Research
Year: 2025
Volume: 6
Issue: 3
Pages: 159-167
Online publication date: 04/10/2025
Acceptance date: 06/07/2025
Date deposited: 27/11/2025
ISSN (electronic): 2719-4523
Publisher: Walter de Gruyter
URL: https://doi.org/10.1515/rir-2025-0019
DOI: 10.1515/rir-2025-0019
Data Access Statement: No additional data is available.
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