ArticleJournal of bone and mineral metabolism2015
Mycobacterium tuberculosis promotes arthritis development through Toll-like receptor 2.
Article in Journal of bone and mineral metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Pooled it
- A Review of Connecting Bioinformatic Techniques to Rheumatoid Arthritis and its Associated Comorbidities.Current rheumatology reviews · 2025Review
- The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023Review
- Differential Diagnosis of Inflammatory Arthropathy Accompanying Active Tuberculosis Infection.Journal of rheumatic diseases · 2022Article
- Tooth extraction in mice administered zoledronate increases inflammatory cytokine levels and promotes osteonecrosis of the jaw.Journal of bone and mineral metabolism · 2021Article
- Role of Infections in the Pathogenesis of Rheumatoid Arthritis: Focus on Mycobacteria.Microorganisms · 2020Review
- IL-17 Production of Neutrophils Enhances Antibacteria Ability but Promotes Arthritis Development During Mycobacterium tuberculosis Infection.EBioMedicine · 2017Article
- New findings of Toll-like receptors involved in Mycobacterium tuberculosis infection.Pathogens and global health · 2017Review
- Cellular and molecular perspectives in rheumatoid arthritis.Seminars in immunopathology · 2017Review
- The nicotinic acetylcholine receptor α7 subunit is an essential negative regulator of bone mass.Scientific reports · 2017Article
- Microbiota, Immune Subversion, and Chronic Inflammation.Frontiers in immunology · 2017Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a multifactorial disease caused by genetic and environmental factors: however, precise molecular mechanisms underlying its pathogenesis remain largely unknown. Treatment of RA patients with disease-modifying biological agents occasionally promotes Mycobacterium tuberculosis infection or recurrence of M. tuberculosis, although how infection promotes arthritis has not been characterized. Here, we found that arthritis phenotypes in a collagen-induced mouse model were evident only when killed M. tuberculosis was co-administered. Treatment of cultured macrophages with killed M. tuberculosis promoted production of IL-6, a major inflammatory cytokine in RA patients, while similar treatment of TLR2-deficient macrophages failed to induce IL-6 expression. Arthritis scores, joint destruction, and serum IL-6 levels were all significantly ameliorated in TLR2-deficient compared with wild-type mice, even in animals treated with killed M. tuberculosis. These results suggest that M. tuberculosis infection enhances arthritis development and that TLR2 could serve as a therapeutic target for some forms of the disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.