Objective Gut microbiota dysbiosis has been implicated in the pathogenesis of autoimmune and immune-mediated arthritis. Biologics may influence gut microbiota composition; however, it is uncertain whether biologics act directly on microbial communities or indirectly through disease modulation and restoration of immune homeostasis. This systematic review explores how biologic therapies modulate gut microbiota in autoimmune arthritis and their potential as biomarkers for treatment response and disease activity. Methods We searched PubMed, Scopus, the Cochrane Library, and the Web of Science (WOS) for studies assessing gut microbiota changes induced by any biologic therapy in immune-mediated or autoimmune arthritis. The outcomes included changes in microbiota and the potential for microbiota as predictive biomarkers for treatment response and disease activity. Results A total of 12 studies were included. Biologic agents, predominantly anti-TNF and IL-17 inhibitors, significantly altered gut microbiota composition and diversity, with most studies showing increased alpha diversity and normalization of beta diversity post-therapy; however, these effects were not uniformly consistent. Treatment restored beneficial shortchain– fatty-acid–producing taxa, including Faecalibacterium prausnitzii , Megamonas , Lachnoclostridium , and Blautia , while reducing inflammatory genera such as Escherichia-Shigella and Klebsiella? . Certain taxa, notably Lachnospiraceae and Megamonas , correlated with clinical improvement and reduced disease activity. Conclusion Biologic therapy modulates gut microbiota composition in autoimmune and immune-mediated arthritis, promoting a shift toward eubiosis. Specific microbial taxa, including Lachnospiraceae , Blautia , and Faecalibacterium prausnitzii , show potential as noninvasive biomarkers for treatment response and disease activity. These findings guide further longitudinal and interventional studies to validate microbial signatures and their clinical applicability.
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Madhumitha et al. (Sun,) studied this question.
www.synapsesocial.com/papers/6994058c4e9c9e835dfd674d — DOI: https://doi.org/10.3899/jrheum.2025-0915
R. Madhumitha
Mohamed Sayed Zaazouee
Arya Akhila Perumangote vasudevan
The Journal of Rheumatology
Cleveland Clinic
University of Connecticut
Texas Tech University
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