ArticleExperimental & molecular medicine2010
TGF-beta-treated antigen presenting cells suppress collagen- induced arthritis through the promotion of Th2 responses.
Article in Experimental & molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 11 citations in OpenAlex.
- Immunotherapy for lung cancer combining the oligodeoxynucleotides of TLR9 agonist and TGF-β2 inhibitor.Cancer immunology, immunotherapy : CII · 2023Article
- Porphyromonas gingivalis oral infection exacerbates the development and severity of collagen-induced arthritis.Arthritis research & therapy · 2013Article
- Interferon alpha inhibits antigen-specific production of proinflammatory cytokines and enhances antigen-specific transforming growth factor beta production in antigen-induced arthritis.Arthritis research & therapy · 2013Article
- Eye-mediated induction of specific immune tolerance to encephalitogenic antigens.CNS neuroscience & therapeutics · 2013Article
- Type II collagen induces peripheral tolerance in BALB/c mice via the generation of CD8+ T regulatory cells.PloS one · 2012Article
- Regulation of B cell activating factor (BAFF) receptor expression by NF-ΚB signaling in rheumatoid arthritis B cells.Experimental & molecular medicine · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Collagen-induced arthritis (CIA) is mediated by self-reactive CD4(+) T cells that produce inflammatory cytokines. TGF-beta(2)-treated tolerogenic antigen-presenting cells (Tol-APCs) are known to induce tolerance in various autoimmune diseases. In this study, we investigated whether collagen-specific Tol-APCs could induce suppression of CIA. We observed that Tol-APCs could suppress the development and severity of CIA and delay the onset of CIA. Treatment of Tol-APCs reduced the number of IFN-gamma- and IL-17-producing CD4(+) T cells and increased IL-4- and IL-5-producing CD4(+) T cells upon collagen antigen stimulation in vitro. The suppression of CIA conferred by Tol-APCs correlated with their ability to selectively induce IL-10 production. We also observed that treatment of Tol-APCs inhibited not only cellular immune responses but also humoral immune responses in the process of CIA. Our results suggest that in vitro-generated Tol-APCs have potential therapeutic value for the treatment of rheumatoid arthritis as well as other autoimmune diseases.
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