ArticleJournal of immunology (Baltimore, Md. : 1950)2017
Soluble CD83 Inhibits T Cell Activation by Binding to the TLR4/MD-2 Complex on CD14
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 62 citations in OpenAlex.
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- CD83 as a novel prognostic biomarker for diffuse large B-cell lymphoma arising in immune deficiency/dysregulation among rheumatoid arthritis patients treated with methotrexate.Journal of clinical and experimental hematopathology : JCEH · 2026Article
- Transmembrane lectins in cancer immunity: emerging drivers of myeloid-mediated immunosuppression.Frontiers in immunology · 2026Review
- The Soluble Cytoplasmic Tail of CD45 (ct-CD45) Regulates Dendritic Cell Activation and Function via TLR4 Signaling.International journal of molecular sciences · 2025Article
- Multilevel Stressors and Systemic and Tumor Immunity in Black and White Women With Breast Cancer.JAMA network open · 2025Article
- Inhibiting CD44-ICD Attenuates LPS-Induced Initiation of Hepatic Inflammation in Septic Mice.International journal of molecular sciences · 2024Article
- Senescence drives immunotherapy resistance by inducing an immunosuppressive tumor microenvironment.Nature communications · 2024Article
- Alternative splicing of modulatory immune receptors in T lymphocytes: a newly identified and targetable mechanism for anticancer immunotherapy.Frontiers in immunology · 2024Review
- Pregnancy-related factors induce immune tolerance through regulation of sCD83 release.Frontiers in immunology · 2024Article
- Mechanism of TLR4-Mediated Anti-Inflammatory Response Induced by Exopolysaccharide from the Probiotic Bacillus subtilis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- CD83 expression characterizes precursor exhausted T cell population.Communications biology · 2023Article
- CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023Review
- Editorial: The key role of Mer receptor tyrosine kinase: where inflammation ends and fibrosis begins.Frontiers in immunology · 2023Article
- Soluble CD83 modulates human-monocyte-derived macrophages toward alternative phenotype, function, and metabolism.Frontiers in immunology · 2023Article
- TGF-β regulates the stem-like state of PD-1+ TCF-1+ virus-specific CD8 T cells during chronic infection.The Journal of experimental medicine · 2022Article
- Tilting the Balance: Therapeutic Prospects of CD83 as a Checkpoint Molecule Controlling Resolution of Inflammation.International journal of molecular sciences · 2022Review
- The soluble CD83 protein prevents bone destruction by inhibiting the formation of osteoclasts and inducing resolution of inflammation in arthritis.Frontiers in immunology · 2022Article
- Monocyte biology conserved across species: Functional insights from cattle.Frontiers in immunology · 2022Article
- Evaluation of Soluble CD90: Potential for Diagnostic Significance in Endometriosis Patients.Disease markers · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transmembrane protein CD83, expressed on APCs, B cells, and T cells, can be expressed as a soluble form generated by alternative splice variants and/or by shedding. Soluble CD83 (sCD83) was shown to be involved in negatively regulating the immune response. sCD83 inhibits T cell proliferation in vitro, supports allograft survival in vivo, prevents corneal transplant rejection, and attenuates the progression and severity of autoimmune diseases and experimental colitis. Although sCD83 binds to human PBMCs, the specific molecules that bind sCD83 have not been identified. In this article, we identify myeloid differentiation factor-2 (MD-2), the coreceptor within the TLR4/MD-2 receptor complex, as the high-affinity sCD83 binding partner. TLR4/MD-2 mediates proinflammatory signal delivery following recognition of bacterial LPSs. However, altering TLR4 signaling can attenuate the proinflammatory cascade, leading to LPS tolerance. Our data show that binding of sCD83 to MD-2 alters this signaling cascade by rapidly degrading IL-1R-associated kinase-1, leading to induction of the anti-inflammatory mediators IDO, IL-10, and PGE
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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.