ArticleArthritis research & therapy2008
Toll-like receptor homolog RP105 modulates the antigen-presenting cell function and regulates the development of collagen-induced arthritis.
Article in Arthritis research & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- The role of CD180 in hematological malignancies and inflammatory disorders.Molecular medicine (Cambridge, Mass.) · 2023Review
- Recent Findings on Thymoquinone and Its Applications as a Nanocarrier for the Treatment of Cancer and Rheumatoid Arthritis.Pharmaceutics · 2021Review
- The Potential Role of RP105 in Regulation of Inflammation and Osteoclastogenesis During Inflammatory Diseases.Frontiers in cell and developmental biology · 2021Review
- Integrating GWAS with bulk and single-cell RNA-sequencing reveals a role for LY86 in the anti-Candida host response.PLoS pathogens · 2020Article
- Toll-Like Receptor-4 Signaling Drives Persistent Fibroblast Activation and Prevents Fibrosis Resolution in Scleroderma.Advances in wound care · 2017Review
- Emerging roles of innate immune signaling and toll-like receptors in fibrosis and systemic sclerosis.Current rheumatology reports · 2015Review
- TLR4 accessory molecule RP105 (CD180) regulates monocyte-driven arteriogenesis in a murine hind limb ischemia model.PloS one · 2014Article
- Article
- Phenotyping of P105-negative B cell subsets in patients with systemic lupus erythematosus.Clinical & developmental immunology · 2012Article
- RP105-negative B cells in systemic lupus erythematosus.Clinical & developmental immunology · 2012Review
- The role of toll-like receptors in rheumatoid arthritis.Current rheumatology reports · 2009Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionRP105 is a Toll-like receptor homolog expressed on B cells, dendritic cells (DCs), and macrophages. We investigated the role of RP105 in the development of collagen-induced arthritis (CIA).
methodsCIA was induced in RP105-deficient DBA/1 mice and the incidence and arthritis index were analyzed. The cytokine production by spleen cells was determined. The functions of the DCs and regulatory T cells (Tregs) from RP105-deficient or control mice were determined by adding these cells to the lymph node cell culture. Arthritis was also induced by incomplete Freund's adjuvant (IFA) plus collagen or by injecting anti-collagen antibody and lipopolysaccharide.
resultsRP105-deficient mice showed accelerated onset of arthritis and increased severity. Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha production by spleen cells from RP105-deficient mice was increased in comparison with that from wild-type mice. The DCs from RP105-deficient mice induced more IFN-gamma production, whereas Tregs from those mice showed less inhibitory effect against IFN-gamma production. RP105-deficient mice also showed more severe arthritis induced by collagen with IFA.
conclusionsThese results indicate that RP105 regulates the antigen-presenting cell function and Treg development, which induced the attenuation of the cell-mediated immune responses and, as a result, suppressed the development of CIA.
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