ArticleJournal of pain research2025
Exploring the Interaction Mechanisms of Antibody-Mediated Immune Responses with Gout and Rheumatoid Arthritis Through a Bidirectional Two-Sample Mendelian Randomization Study.
Article in Journal of pain research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
- Spatiotemporal immune gradients in gout: immune response-driven activation of the NLRP3-IL-1β axis and its transition to trained immunity.Frontiers in immunology · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Gout and Rheumatoid arthritis (RA) are two prevalent non-infectious inflammatory joint diseases that can occur independently or concurrently. The effects and mechanisms related to antibody-mediated immune responses and both Gout and RA remain unclear. The research seeks to investigate the potential causal association and offer a novel perspective for their prevention and treatment strategies. Methods: The study employed the bidirectional two-sample Mendelian randomization (MR) analysis for investigation. Datasets comprising 46 antibody-mediated immune responses, as well as those for Gout and RA, were curated from published genome-wide association studies (GWAS). For the causality analysis, methods such as Inverse Variance Weighted (IVW), Weighted Median, Simple Mode, MR-Egger, and Weighted Mode were utilized. We chose MR pleiotropy residual sum and outlier (MR-PRESSO), IVW, MR-Egger, and Leave-one-out for sensitivity analysis to enhance the reliability of the results. Results: We meticulously excluded the results that exhibited pleiotropy and instability. Finally, four antibody-mediated immune responses have been found as causal factors in the development of Gout: Anti-chlamydia trachomatis IgG seropositivity, Anti-human herpes virus 6 IE1B IgG seropositivity, Helicobacter pylori GroEL antibody levels, and Polyomavirus 2 JC VP1 antibody levels; Two antibody-mediated immune responses influence RA causally: BK polyomavirus VP1 antibody levels, and Helicobacter pylori Catalase antibody levels. In the reverse analysis, three antibody-mediated immune responses could be influenced by Gout: BK polyomavirus VP1 antibody levels, Chlamydia trachomatis tarp-D F2 antibody levels, and Varicella zoster virus glycoproteins E and I antibody levels; Two antibody-mediated immune responses could be causally affected by RA: Anti-human herpes virus 7 IgG seropositivity, and Merkel cell polyomavirus VP1 antibody levels. Conclusion: The research indicated that antibody-mediated immune responses establish a causal link with this two non-infectious inflammatory joint diseases: Gout and RA, offering new avenues and perspectives for the future prophylaxis and treatment of diseases from an immunological standpoint.
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