Rheumatoid arthritis and the gut microbiota: From microbial dysbiosis to immune modulation - A Narrative Review
- 1Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan Iran
Abstract
Background: Rheumatoid arthritis (RA) is a chronic autoimmune condition characterised by synovial inflammation, joint dysfunction, and systemic comorbidities. Although genetic predisposition is a major contributor to RA, environmental and host-related factors, including gut microflora, are increasingly recognised as important contributors to disease initiation and progression. Dysregulation of tolerogenic pathways leads to alterations in gut microbiota composition and function, which may manifest as a state known as dysbiosis during eATD progression; this state has been associated with aberrant T-cell (CD8+ or CD4+) and B-cell responses, as well as systemic inflammation. Methods: In this review, we summarise recent research articles (2019-2025) examining the interplay between the gut microbiota, mucosal immunity, and RA development. In particular, we highlight how microbes colonise the human gut and influence downstream immune responses, including Th17 cell differentiation or reduced regulatory T-cell numbers, species-specific activation of antigen-presenting cells, and immune modulation mediated by microbial metabolites. Results: Finally, we briefly review evidence supporting gut barrier dysfunction and microbial translocation as drivers of autoimmunity through molecular mimicry. Furthermore, the therapeutic potential of gliadin-dependent reactivity is contrasted with approaches targeting the gut microbiome, including probiotics, faecal transplantation, dietary manipulation, and disease-modifying antirheumatic drugs (DMARDs). Understanding the gut-joint axis may provide new biomarkers, preventive strategies, and microbiota-targeted therapies for RA. Conclusion: The gut microbiota plays a key role in RA pathogenesis by modulating immune responses. Dysbiosis promotes loss of tolerance, Th17 and B-cell activation, and systemic inflammation through barrier dysfunction and metabolite imbalance. Microbiome-targeted approaches may offer preventive, diagnostic, and therapeutic opportunities, warranting further longitudinal and clinical studies.
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BibTeX
@article{kouhsari2026rheumatoid,
title = {{Rheumatoid arthritis and the gut microbiota: From microbial dysbiosis to immune modulation - A Narrative Review}},
author = {Ebrahim Kouhsari and Koushan Sineh Sepehr},
journal = {Medical Laboratory Journal},
year = {2026},
month = jul,
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Rheumatoid arthritis and the gut microbiota: From microbial dysbiosis to immune modulation - A Narrative Review
AU - Ebrahim Kouhsari
AU - Koushan Sineh Sepehr
PY - 2026
DA - 2026/07/01
JO - Medical Laboratory Journal
AB - Background: Rheumatoid arthritis (RA) is a chronic autoimmune condition characterised by synovial inflammation, joint dysfunction, and systemic comorbidities. Although genetic predisposition is a major contributor to RA, environmental and host-related factors, including gut microflora, are increasingly recognised as important contributors to disease initiation and progression. Dysregulation of tolerogenic pathways leads to alterations in gut microbiota composition and function, which may manifest as a state known as dysbiosis during eATD progression; this state has been associated with aberrant T-cell (CD8+ or CD4+) and B-cell responses, as well as systemic inflammation. Methods: In this review, we summarise recent research articles (2019-2025) examining the interplay between the gut microbiota, mucosal immunity, and RA development. In particular, we highlight how microbes colonise the human gut and influence downstream immune responses, including Th17 cell differentiation or reduced regulatory T-cell numbers, species-specific activation of antigen-presenting cells, and immune modulation mediated by microbial metabolites. Results: Finally, we briefly review evidence supporting gut barrier dysfunction and microbial translocation as drivers of autoimmunity through molecular mimicry. Furthermore, the therapeutic potential of gliadin-dependent reactivity is contrasted with approaches targeting the gut microbiome, including probiotics, faecal transplantation, dietary manipulation, and disease-modifying antirheumatic drugs (DMARDs). Understanding the gut-joint axis may provide new biomarkers, preventive strategies, and microbiota-targeted therapies for RA. Conclusion: The gut microbiota plays a key role in RA pathogenesis by modulating immune responses. Dysbiosis promotes loss of tolerance, Th17 and B-cell activation, and systemic inflammation through barrier dysfunction and metabolite imbalance. Microbiome-targeted approaches may offer preventive, diagnostic, and therapeutic opportunities, warranting further longitudinal and clinical studies.
SN - 2538-4449
ER -