ArticleFrontiers in immunology2019
Soluble CD83 Triggers Resolution of Arthritis and Sustained Inflammation Control in IDO Dependent Manner.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Tunable wrinkled topographies direct dendritic cell maturation and immune phenotypes.Acta biomaterialia · 2026Article
- Reduced tolerogenic factor sCD83 in NMOSD and relapsing MOGAD: a potential new therapeutic pathway.Frontiers in immunology · 2025Article
- Resveratrol Attenuates Rheumatoid Arthritis Induce Neutrophil Extracellular Traps via TLR-4 Mediated Inflammation in C57BL/6 Mice.Physiological research · 2024Article
- Pregnancy-related factors induce immune tolerance through regulation of sCD83 release.Frontiers in immunology · 2024Article
- The Epigenetic Reader Protein SP140 Regulates Dendritic Cell Activation, Maturation and Tolerogenic Potential.Current issues in molecular biology · 2023Article
- CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023Review
- CD83 expressed by macrophages is an important immune checkpoint molecule for the resolution of inflammation.Frontiers in immunology · 2023Article
- Soluble CD83 modulates human-monocyte-derived macrophages toward alternative phenotype, function, and metabolism.Frontiers in immunology · 2023Article
- Tilting the Balance: Therapeutic Prospects of CD83 as a Checkpoint Molecule Controlling Resolution of Inflammation.International journal of molecular sciences · 2022Review
- Anti-Mouse CD83 Monoclonal Antibody Targeting Mature Dendritic Cells Provides Protection Against Collagen Induced Arthritis.Frontiers in immunology · 2022Article
- Soluble CD83 improves and accelerates wound healing by the induction of pro-resolving macrophages.Frontiers in immunology · 2022Article
- The soluble CD83 protein prevents bone destruction by inhibiting the formation of osteoclasts and inducing resolution of inflammation in arthritis.Frontiers in immunology · 2022Article
- Intestinal Epithelial Cell-Derived CD83 Contributes to Regulatory T-Cell Generation and Inhibition of Food Allergy.Journal of innate immunity · 2021Article
- Amino Acid Metabolism in Rheumatoid Arthritis: Friend or Foe?Biomolecules · 2020Review
- The CD83 Molecule - An Important Immune Checkpoint.Frontiers in immunology · 2020Review
- Soluble CD83 alleviates experimental allergic rhinitis through modulating antigen-specific Th2 cell property.International journal of biological sciences · 2020Article
- CD83 orchestrates immunity toward self and non-self in dendritic cells.JCI insight · 2019Article
- Soluble CD83: a proresolving mediator in inflammatory arthritis?Nature reviews. Rheumatology · 2019Article
- CD83: Activation Marker for Antigen Presenting Cells and Its Therapeutic Potential.Frontiers in immunology · 2019Review
- Soluble CD83 Accelerates Wound Healing and Attenuates Inflammatory Responses Induced by Chronic Wound Fluid in a Human 3D in Vitro Wound Healing Model.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interference with autoimmune-mediated cytokine production is a key yet poorly developed approach to treat autoimmune and inflammatory diseases such as rheumatoid arthritis. Herein, we show that soluble CD83 (sCD83) enhances the resolution of autoimmune antigen-induced arthritis (AIA) by strongly reducing the expression levels of cytokines such as IL-17A, IFNγ, IL-6, and TNFα within the joints. Noteworthy, also the expression of RANKL, osteoclast differentiation, and joint destruction was significantly inhibited by sCD83. In addition, osteoclasts which were cultured in the presence of synovial T cells, derived from sCD83 treated AIA mice, showed a strongly reduced number of multinuclear large osteoclasts compared to mock controls. Enhanced resolution of arthritis by sCD83 was mechanistically based on IDO, since inhibition of IDO by 1-methyltryptophan completely abrogated sCD83 effects on AIA. Blocking experiments, using anti-TGF-β antibodies further revealed that also TGF-β is mechanistically involved in the sCD83 induced reduction of bone destruction and cartilage damage as well as enhanced resolution of inflammation. Resolution of arthritis was associated with increased numbers of regulatory T cells, which are induced in a sCD83-IDO-TGF-β dependent manner. Taken together, sCD83 represents an interesting approach for downregulating cytokine production, inducing regulatory T cells and inducing resolution of autoimmune arthritis.
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