ReviewFrontiers in microbiology2016
How Rheumatoid Arthritis Can Result from Provocation of the Immune System by Microorganisms and Viruses.
Review in Frontiers in microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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
39 citing papers in PubMed, 70 citations in OpenAlex.
- Joint Tissues: Convergence and Divergence of the Pathogenetic Mechanisms of Rheumatoid Arthritis and Osteoarthritis.International journal of molecular sciences · 2025Review
- Environmental and Lifestyle Factors in the Risk and Prevention of Rheumatoid Arthritis: A Narrative Review.Cureus · 2025Review
- The Gut Feeling: The Role of Gut Microbiome in Orthopedics.Journal of orthopaedic case reports · 2025Article
- Citrullinated peptides as drug candidates for rheumatoid arthritis.Frontiers in immunology · 2025Review
- Molecular Regulation of Bone Turnover in Juvenile Idiopathic Arthritis: Animal Models, Cellular Features and TNFα.Frontiers in bioscience (Landmark edition) · 2024Review
- Therapeutic Potential of Plant-Derived Compounds and Plant Extracts in Rheumatoid Arthritis-Comprehensive Review.Antioxidants (Basel, Switzerland) · 2024Review
- The Lung in Rheumatoid Arthritis-Friend or Enemy?International journal of molecular sciences · 2024Review
- At Early Rheumatoid Arthritis Stage, the Infectious Spectrum Is Driven by Non-Familial Factors and Anti-CCP Immunization.Journal of clinical medicine · 2024Article
- Distinct oral DNA viral signatures in rheumatoid arthritis: a Pilot study.Journal of oral microbiology · 2024Article
- Review
- Characteristics of the (Auto)Reactive T Cells in Rheumatoid Arthritis According to the Immune Epitope Database.International journal of molecular sciences · 2023Review
- Multi-omics analysis identifies IgG2b class-switching with ALCAM-CD6 co-stimulation in joint-draining lymph nodes during advanced inflammatory-erosive arthritis.Frontiers in immunology · 2023Article
- Anti-Citrullinated Peptide Antibodies Control OralInternational journal of molecular sciences · 2022Article
- Interplay of Environmental, Individual and Genetic Factors in Rheumatoid Arthritis Provocation.International journal of molecular sciences · 2022Review
- Review
- Editorial: Epigenetic aspects of autoimmune diseases.Frontiers in cell and developmental biology · 2022Article
- Illumination on Chemical Compounds from Qufeng Zhitong Capsule and Its Potential Pharmacological Mechanism against Rheumatoid Arthritis Based on UHPLC/Q-Orbitrap-MS Combined with Network Pharmacology Analysis.International journal of analytical chemistry · 2022Article
- SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases.Journal of translational autoimmunity · 2022Article
- Identification of viral-mediated pathogenic mechanisms in neurodegenerative diseases using network-based approaches.Briefings in bioinformatics · 2021Article
- A Bayesian Model to Analyze the Association of Rheumatoid Arthritis With Risk Factors and Their Interactions.Frontiers in public health · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of rheumatoid arthritis (RA), similar to development of a majority of inflammatory and autoimmune disorders, is largely due to an inappropriate or inadequate immune response to environmental challenges. Among these challenges, infectious agents are the undisputed leaders. Since the 1870s, an impressive list of microorganisms suspected of provoking RA has formed, and the list is still growing. Although a definite causative link between a specific infectious agent and the disease has not been established, several arguments support such a possibility. First, in the absence of a defined pathogen, the spectrum of triggering agents may include polymicrobial communities or the cumulative effect of several bacterial/viral factors. Second, the range of infectious episodes (i.e., clinical manifestations caused by pathogens) may vary in the process of RA development from preclinical to late-stage disease. Third, infectious agents might not trigger RA in all cases, but trigger it in a certain subset of the cases, or the disease onset may arise from an unfortunate combination of infections along with, for example, psychological stress and/or chronic joint tissue microtrauma. Fourth, genetic differences may have a role in the disease onset. In this review, two aspects of the problem of "microorganisms and RA" are debated. First, is there an acquired immune deficiency and, in turn, susceptibility to infections in RA patients due to the too frequent and too lengthy infections, which at last break the tolerance of self antigens? Or, second, is there a congenital deficiency in tolerance and inflammation control, which may occur even with ordinary infection frequency and duration?
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