Affinage

CD83

CD83 antigen · UniProt Q01151

Length
205 aa
Mass
23.0 kDa
Annotated
2026-04-28
100 papers in source corpus 30 papers cited in narrative 30 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CD83 is an immunoglobulin superfamily glycoprotein that functions as a central regulator of antigen presentation and immune tolerance across dendritic cells, B cells, regulatory T cells, and microglia. Its transmembrane domain stabilizes surface MHC class II and CD86 by antagonizing MARCH1-mediated ubiquitination in dendritic cells and March8-mediated ubiquitination in cortical thymic epithelial cells, a mechanism essential for CD4+ T cell thymic selection and peripheral T cell priming (PMID:21220452, PMID:27503071, PMID:11955430). Soluble CD83, generated by both alternative splicing and proteolytic shedding, exerts immunosuppressive effects by binding MD-2 in the TLR4/MD-2 complex on monocytes to induce IDO, IL-10, and PGE2 production, and CD83 expression in Tregs, DCs, and microglia restrains inflammatory responses, as conditional deletion in each lineage results in exacerbated autoimmunity (PMID:28193829, PMID:29875316, PMID:31527313, PMID:37528070). CD83 protein levels are regulated post-translationally by glycosylation-dependent trafficking from preformed intracellular stores, by GRAIL-mediated ubiquitination at K168/K183 in anergic T cells, and by HSV-1 ICP0-directed proteasomal degradation as a viral immune evasion strategy (PMID:15320871, PMID:19542455, PMID:17428858).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2001 Medium

    Establishing that CD83 has a ligand-binding function: the extracellular domain was shown to engage a 72 kDa sialic acid-dependent counter-receptor on monocytes and activated CD8+ T cells, and that membrane CD83 is shed to produce a soluble form detectable in serum, framing CD83 as both a membrane receptor and a released immunomodulator.

    Evidence CD83-Ig fusion protein binding assays with neuraminidase treatment; sCD83-specific ELISA with cycloheximide blockade showing shedding mechanism

    PMID:11238630 PMID:11431426

    Open questions at the time
    • Identity of the 72 kDa counter-receptor was not determined
    • Protease responsible for shedding not identified
    • Physiological relevance of serum sCD83 levels not established
  2. 2002 High

    Demonstrating that CD83 is non-redundantly required for CD4+ T cell development: CD83-knockout mice showed a specific block in CD4+ single-positive thymocyte generation, and the defect mapped to thymic stromal cells rather than thymocytes, establishing CD83 as essential for thymic positive selection.

    Evidence CD83-knockout mice with bone marrow and thymocyte adoptive transfer experiments

    PMID:11955430

    Open questions at the time
    • Molecular mechanism by which CD83 promotes CD4 selection was unknown
    • Whether CD83 acted on MHC II stability or via a signaling pathway was unresolved
  3. 2002 Medium

    Defining the transcriptional regulation of CD83: the promoter was shown to be NF-κB-dependent and TNF-α-inducible, and EBV LMP1 was later shown to activate CD83 transcription through the same NF-κB element, linking viral latency to CD83 upregulation in B cells.

    Evidence Promoter deletion/reporter assays with EMSA; LMP1 mutant and chimeric receptor reporter assays

    PMID:12182451 PMID:12857898

    Open questions at the time
    • Other transcription factors contributing to cell-type-specific CD83 expression were not characterized
    • Epigenetic regulation not examined
  4. 2005 High

    Resolving how CD83 surface expression is so rapidly induced: preformed CD83 protein exists intracellularly in immature DCs and is trafficked to the surface upon activation through a glycosylation-dependent, secretory-pathway mechanism that does not require new protein synthesis, revealing post-translational rather than transcriptional control as the primary switch.

    Evidence Brefeldin A, cycloheximide, and tunicamycin treatment of DCs; PNGase F digestion; flow cytometry and Western blot

    PMID:15320871

    Open questions at the time
    • Glycosyltransferases responsible for the 37→50 kDa modification not identified
    • Signal triggering ER-to-surface trafficking not defined
  5. 2005 Medium

    Characterizing alternative forms of soluble CD83: alternative splicing was identified as a second source (beyond shedding) of soluble CD83, and the soluble protein was shown to potently inhibit T cell proliferation, while structural analysis revealed CD83 forms a disulfide-linked dimer via C129, though dimerization is dispensable for immunosuppressive function.

    Evidence RT-PCR cloning of splice variants; recombinant sCD83 in MLR; C129S mutagenesis with non-reducing SDS-PAGE

    PMID:15721284 PMID:15905506

    Open questions at the time
    • Relative contributions of splicing versus shedding to sCD83 pools in vivo unknown
    • Whether dimerization affects receptor binding affinity not tested
  6. 2006 High

    Uncovering a post-transcriptional regulatory circuit: CD83 mRNA contains a cis-acting element bound by HuR, which mediates CRM1/Nup214-dependent nuclear export; the HuR co-factor APRIL/ANP32B further promotes this export in a phosphorylation-dependent manner, establishing mRNA export as a rate-limiting step in CD83 expression.

    Evidence HuR and APRIL RNAi; leptomycin B treatment; dominant-negative Nup214; phosphorylation site mutagenesis

    PMID:16484227 PMID:17178712

    Open questions at the time
    • Whether this mRNA export mechanism operates in all CD83-expressing cell types not tested
    • Kinase phosphorylating APRIL T244 not identified
  7. 2007 Medium

    Identifying viral immune evasion targeting CD83: HSV-1 ICP0 was shown to drive proteasomal degradation of CD83 in mature DCs, initially attributed to ICP0's RING finger E3 ligase activity, though a subsequent study found degradation to be independent of this domain, leaving the precise mechanism debated.

    Evidence HSV-1 ICP0 deletion/RING mutants; proteasome inhibitor rescue; FACS and Western blot in mDCs and 293T cells

    PMID:17428858 PMID:24643878

    Open questions at the time
    • Whether ICP0 directly ubiquitinates CD83 or recruits another E3 ligase is unresolved
    • The contradictory findings on RING domain requirement have not been reconciled
  8. 2009 High

    Defining a T cell-intrinsic ubiquitin-dependent degradation pathway for CD83: GRAIL was identified as the E3 ligase ubiquitinating CD83 at K168 and K183 for proteasomal degradation in CD4+ T cells, providing a molecular mechanism for CD83 downregulation during T cell anergy.

    Evidence Retroviral GRAIL transduction; site-directed mutagenesis of CD83 lysines; in vitro ubiquitination assay; proteasome inhibitor rescue

    PMID:19542455

    Open questions at the time
    • Whether GRAIL targets CD83 in vivo during anergy induction not demonstrated
    • Signals coupling anergy to GRAIL-CD83 interaction not defined
  9. 2011 High

    Solving the molecular mechanism of CD83 in MHC II stabilization: the transmembrane domain of CD83 was shown to block MARCH1-mediated ubiquitination and degradation of MHC II and CD86 on DCs, establishing CD83 as a competitive inhibitor of MARCH E3 ligases rather than a conventional signaling receptor.

    Evidence ENU-induced CD83 transmembrane mutant mice; genetic epistasis with MARCH1 knockout; functional rescue

    PMID:21220452

    Open questions at the time
    • Whether CD83 TMD directly binds MARCH1 TMD or acts indirectly not determined
    • Stoichiometry of CD83–MARCH1 interaction unknown
  10. 2011 Medium

    Identifying the signal inducing CD83 on B cells and a downstream immunosuppressive effector: CD40 engagement by T cells was shown to drive CD83 upregulation on B cells, and membrane CD83 engagement on monocytes triggers COX-2-dependent PGE2 production via NF-κB, mediating T cell suppression.

    Evidence Anti-CD40L blockade and transwell experiments; COX-2 inhibitor NS-398 treatment with cytokine and proliferation assays

    PMID:21277328 PMID:22065790

    Open questions at the time
    • Direct receptor for membrane CD83 on monocytes not identified at this stage
    • Whether PGE2 pathway operates in vivo not shown
  11. 2014 Medium

    Demonstrating that membrane CD83 actively promotes T cell activation through calcium signaling and that homotypic DC–DC CD83 interactions suppress inflammation via p38α: these findings revealed CD83 has dual context-dependent functions—costimulatory in DC–T cell contact and inhibitory in DC–DC contact.

    Evidence CD83 siRNA and anti-CD83 antibody with Fluo-4-AM calcium imaging; CD83 cytoplasmic truncation mutants with p38α phosphorylation assays in colitis models

    PMID:24436459 PMID:25204675

    Open questions at the time
    • T cell receptor for membrane CD83 not identified
    • Whether cytoplasmic domain signals directly or via adaptor proteins unknown
  12. 2016 High

    Extending the MARCH-antagonism model to thymic selection: in cortical thymic epithelial cells, CD83 TMD antagonizes March8 (not March1) to stabilize MHC II, directly explaining the CD4+ T cell selection defect in CD83-knockout mice identified 14 years earlier.

    Evidence Cd83−/− cTEC reconstitution; March8 ablation rescue; ubiquitination-resistant MHC II variant rescue in CD83-deficient thymus

    PMID:27503071

    Open questions at the time
    • Whether CD83 TMD binds March8 directly or competes for substrate access not resolved
    • Structural basis of E3 ligase selectivity (March1 in DCs vs March8 in cTECs) unknown
  13. 2016 Medium

    Establishing a B cell-intrinsic role for CD83: B cell-specific CD83 deletion revealed impaired MHC II and CD86 upregulation, defective germinal center responses, and dysregulated IgE production, extending the MARCH-antagonism paradigm to the B cell lineage.

    Evidence B cell-specific CD83 conditional KO mice; mixed bone marrow chimeras; immunization and infection models

    PMID:26983787

    Open questions at the time
    • Which MARCH family member CD83 antagonizes in B cells not determined
    • Whether GC phenotype is solely due to MHC II instability or additional pathways unclear
  14. 2017 High

    Identifying the receptor for soluble CD83: sCD83 was shown to bind MD-2 within the TLR4/MD-2 complex on monocytes, triggering IRAK-1 degradation and inducing IDO, IL-10, and PGE2, providing a unified molecular explanation for the immunosuppressive activity of sCD83.

    Evidence Direct binding assays identifying MD-2; IRAK-1 degradation kinetics; COX-2 inhibition; T cell proliferation assays

    PMID:28193829

    Open questions at the time
    • Whether sCD83 competes with LPS for MD-2 binding not addressed
    • Crystal structure of sCD83–MD-2 complex not available
  15. 2018 Medium

    Demonstrating Treg-intrinsic requirement for CD83: conditional Treg-specific CD83 deletion caused loss of Treg differentiation markers and a pro-inflammatory phenotype, establishing that CD83 is not merely a Treg marker but functions cell-autonomously in Treg identity and suppressive capacity.

    Evidence Treg-specific conditional CD83 KO mice; scRNA-seq; autoimmunity phenotyping

    PMID:29875316

    Open questions at the time
    • Whether Treg CD83 acts via MARCH antagonism or an independent mechanism not determined
    • Direct target of CD83 signaling within Tregs unknown
  16. 2019 Medium

    Extending CD83's immune-regulatory role to DCs and demonstrating sCD83 therapeutic mechanism: DC-specific CD83 deletion caused hyperactivated DCs with excess IL-2 and IL-12 production leading to exacerbated autoimmunity, while sCD83 resolved arthritis via IDO- and TGF-β-dependent Treg induction.

    Evidence DC-specific CD83 conditional KO in EAE and infection models; sCD83 treatment in antigen-induced arthritis with IDO inhibitor and anti-TGF-β blockade

    PMID:31001257 PMID:31527313

    Open questions at the time
    • Whether DC CD83 restraint operates through MARCH1 antagonism or additional pathways not fully resolved
    • Pharmacokinetics and in vivo receptor engagement of sCD83 not characterized
  17. 2023 Medium

    Extending CD83 immune-regulatory function to the CNS: microglia-specific CD83 deletion led to over-activated microglia and exacerbated neuroinflammation in EAE, demonstrating that CD83's tolerance-promoting role extends beyond classical adaptive immune cells to CNS-resident innate immune cells.

    Evidence Conditional microglia-specific CD83 KO mice; EAE model; single-cell RNA-seq; CNS infiltrate analysis

    PMID:37528070

    Open questions at the time
    • Whether microglial CD83 antagonizes a MARCH ligase or acts via a distinct mechanism unknown
    • Microglial CD83 ligand or signaling partners not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of CD83 transmembrane domain interaction with MARCH E3 ligases, the identity of the membrane CD83 counter-receptor on T cells, whether MARCH antagonism fully explains CD83 function in Tregs and microglia, and the in vivo therapeutic potential of sCD83 via the MD-2 axis.
  • No structural model of CD83 TMD–MARCH interaction exists
  • T cell counter-receptor for membrane CD83 remains unidentified
  • Cell-type-specific mechanisms beyond MARCH antagonism are undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0048018 receptor ligand activity 2 GO:0098631 cell adhesion mediator activity 1
Localization
GO:0005886 plasma membrane 4 GO:0005576 extracellular region 3 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-168256 Immune System 7 R-HSA-162582 Signal Transduction 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-1266738 Developmental Biology 2
Partners
CD40ELAVL1LY96MARCH1MARCH8RNF128

Evidence

Reading pass · 30 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 The transmembrane domain of CD83 blocks IL-10-driven MARCH1-mediated ubiquitination and degradation of MHC class II and CD86 on dendritic cells, thereby stabilizing surface MHC II and CD86 expression. N-ethyl-N-nitrosourea-induced mouse mutation eliminating CD83 transmembrane region; genetic epistasis with MARCH1; functional rescue experiments The Journal of experimental medicine High 21220452
2016 In cortical thymic epithelial cells (cTECs), CD83's transmembrane domain is necessary and sufficient for thymic CD4 T cell selection by antagonizing the E3 ubiquitin ligase March8 (not March1) to stabilize MHC II on cTECs. Viral reconstitution of CD83 gene function in thymic epithelial cells; Cd83-/- mice rescued by ablating March8; ubiquitination-resistant MHCII variant rescue The Journal of experimental medicine High 27503071
2002 CD83 expression by thymic epithelial and dendritic cells is required for CD4+ single-positive thymocyte development; CD83-deficient mice show a specific block in CD4+ T cell generation, and wild-type thymocytes fail to develop into CD4+ T cells in CD83-/- hosts. CD83-knockout mice; bone marrow and thymocyte transfer experiments Cell High 11955430
2017 Soluble CD83 (sCD83) binds to MD-2, the co-receptor of the TLR4/MD-2 complex on CD14+ monocytes, rapidly degrades IRAK-1, and induces anti-inflammatory mediators IDO, IL-10, and PGE2 in a COX-2-dependent manner, thereby suppressing T cell proliferation and IL-2 secretion. Binding assays identifying MD-2 as sCD83 partner; IRAK-1 degradation assays; pharmacological inhibition of COX-2; T cell proliferation assays Journal of immunology High 28193829
2007 HSV-1 immediate-early protein ICP0 drives proteasome-mediated degradation of CD83 in mature dendritic cells, with the RING finger E3 ubiquitin ligase activity of ICP0 required; proteasome inhibition restores CD83 surface expression. HSV-1 ICP0 deletion mutant infection; ICP0/CD83 co-transfection in 293T cells; RING finger mutant ICP0; proteasome inhibitor treatment; FACS and Western blot Journal of virology High 17428858
2014 HSV-1 ICP0 alone is sufficient to degrade CD83 in mature dendritic cells, but this degradation is independent of ICP0's E3 ubiquitin ligase domain and independent of lysine ubiquitination, suggesting a distinct proteasomal degradation mechanism. Expression of ICP0 mutants lacking E3 ubiquitin ligase domain; E1 activating enzyme inhibitor; infection experiments in mDCs The Journal of general virology Medium 24643878
2015 HSV-1 L particles (containing viral proteins but lacking capsid and DNA) transfer viral proteins from infected mature dendritic cells to uninfected bystander DCs, inducing CD83 downmodulation in the absence of productive infection. L particle isolation and incubation with uninfected mDCs; transwell exclusion of phagocytosis; FACS analysis of CD83 Journal of virology Medium 26311871
2009 The transmembrane RING finger E3 ubiquitin ligase GRAIL ubiquitinates CD83 on lysine residues K168 and K183 (but not K192) in its cytoplasmic domain, targeting it for 26S proteasome-mediated degradation in CD4+ T cells; GRAIL-mediated CD83 downregulation requires intact extracellular protease-associated and RING domains. Retroviral GRAIL transduction; RNA interference knockdown; site-directed mutagenesis of CD83 lysines; proteasome inhibitor assays; in vitro ubiquitination Journal of immunology High 19542455
2004 HCMV infection of mature monocyte-derived dendritic cells causes shedding of CD83 from the cell surface into the supernatant as soluble CD83, and this soluble CD83 accounts for the immunosuppressive activity of infected DC supernatants on normal DC-mediated T cell stimulation. CD83 immunodepletion from HCMV-infected moDC supernatants; virion-depleted supernatant transfer; Western blot; ELISA Blood Medium 14962896
2001 CD83 functions as an adhesion receptor; its soluble extracellular domain binds to monocytes and a subset of activated CD8+ T cells via a 72 kDa sialic acid-dependent counter-receptor; neuraminidase treatment abolishes binding. CD83-Ig fusion protein binding assays; immunoprecipitation of 72 kDa counter-receptor; neuraminidase treatment; CD83-transfected carcinoma cell adhesion assay Journal of immunology Medium 11238630
2001 Soluble CD83 released from activated dendritic cells and B lymphocytes is generated by shedding of membrane CD83 (inhibition of protein synthesis does not prevent short-term sCD83 release); it is detectable in normal human serum. sCD83-specific ELISA; Western blotting; cycloheximide inhibition of protein synthesis; mCD83+ and mCD83- cell line comparison International immunology Medium 11431426
2005 CD83 is preformed as an intracellular protein in immature DCs, monocytes, and macrophages; its rapid surface expression upon activation is post-translationally regulated, requires glycosylation (blocked by tunicamycin), and occurs via a brefeldin A-sensitive (secretory pathway) but cycloheximide-insensitive (pre-existing protein) mechanism. Mature DCs express a 50 kDa glycoform while immature cells express a 37 kDa form. Western blotting; indirect immunofluorescence; brefeldin A, cycloheximide, and tunicamycin treatment; PNGase F digestion; flow cytometry The Biochemical journal High 15320871
2006 CD83 mRNA contains a novel cis-acting post-transcriptional regulatory element in its coding region that binds the RNA-binding protein HuR; HuR is required for cytoplasmic accumulation of CD83 mRNA via the CRM1 nuclear export pathway, and this process depends on the nucleoporin Nup214/CAN. RNA interference knockdown of HuR; transient transfection with CD83 cis-element constructs; leptomycin B (CRM1 inhibitor) treatment; dominant-negative Nup214/CAN overexpression; RNA stability assays The Journal of biological chemistry High 16484227
2006 The HuR ligand APRIL (ANP32B) contributes to nuclear export and subsequent translation of CD83 mRNA; phosphorylation of APRIL at threonine 244 regulates its nuclear export, and APRIL knockdown reduces cytoplasmic CD83 mRNA levels. RNA interference knockdown of APRIL; identification of NLS and NES of APRIL; phosphorylation site mapping by mutagenesis; subcellular fractionation The Journal of biological chemistry Medium 17178712
2005 CD83 can be expressed as soluble forms generated by alternative splicing of CD83 mRNA; at least one splice variant is efficiently translated into protein, and recombinant soluble CD83 strongly inhibits T cell proliferation in mixed lymphocyte reactions. RT-PCR cloning and sequence analysis of CD83 transcripts from PBMCs; recombinant protein expression; MLR inhibition assays Journal of immunology Medium 15905506
2005 CD83 is a disulfide-linked dimer; the fifth cysteine residue at amino acid position 129 in the extracellular Ig domain mediates dimerization via an intermolecular disulfide bond, and a C129S mutant monomeric form retains inhibitory activity on DC maturation and allogeneic T cell stimulation in MLR. Recombinant mutagenesis (C129S substitution); non-reducing SDS-PAGE; MLR assays; DC maturation assays Biochemical and biophysical research communications Medium 15721284
2002 The CD83 promoter contains four SP1 binding sites and one NF-κB element; NF-κB factors specifically bind the NF-κB element (confirmed by EMSA), and promoter activity is inducible by TNF-α in a manner strictly dependent on the intact NF-κB element. Promoter deletion constructs; luciferase reporter assays; electrophoretic mobility shift assays (EMSA); TNF-α stimulation Immunobiology Medium 12182451
2003 EBV latent membrane protein 1 (LMP1) induces CD83 expression in B cells via NF-κB activation; LMP1 mutant studies and luciferase reporter assays with the CD83 promoter demonstrated NF-κB dependence; signaling through CD40, TNF-R1, or TNF-R2 intracellular domains fused to LMP1 transmembrane domain similarly activates the CD83 promoter. Inducible LMP1 expression system (NGFR-LMP1 fusion); luciferase reporter assays with CD83 promoter and LMP1 mutants; EBNA2-inducible LCL system Journal of virology Medium 12857898
2011 CD83 on monocytes, when stimulated by CD83 (membrane CD83 on DCs or T cells), induces COX-2-dependent PGE2 production via NF-κB activation, and this PGE2 mediates T cell suppression (inhibiting IL-2 and IFN-γ); COX-2-selective inhibitor NS-398 fully prevented CD83-triggered T cell inhibition. COX-2 inhibitor (NS-398) treatment; NF-κB pathway analysis; ELISA for PGE2 and cytokines; T cell proliferation assays with monocyte co-cultures Proceedings of the National Academy of Sciences of the United States of America Medium 22065790
2014 CD83 homotypic interactions between dendritic cells (via cell-cell contact) inhibit pro-inflammatory responses by suppressing p38α phosphorylation in the MAPK pathway; CD83 cytoplasmic truncation or knockdown abolishes this homotypic inhibitory signaling. DC conditional knockout of CD83; CD83 overexpression; CD83 knockdown; cytoplasmic truncation mutants; p38α phosphorylation assays; in vitro and in vivo colitis models Mucosal immunology Medium 25204675
2007 CD83 knockdown by siRNA in human monocyte-derived DCs significantly reduces DC-mediated T cell proliferation and alters cytokine expression during T cell priming, demonstrating CD83's role as an enhancer of T cell stimulatory capacity. siRNA electroporation into immature DCs; flow cytometry; allogeneic T cell proliferation assays; cytokine measurements Journal of immunology Medium 17442926
2008 Retroviral transduction of CD83 into naive CD4+CD25- T cells induces a regulatory phenotype including Foxp3 expression; CD83+Foxp3+ T cells suppress contact hypersensitivity and prevent EAE in vivo, reducing IFN-γ and IL-17 while increasing IL-10. Retroviral transduction of CD83 into T cells; adoptive transfer into EAE and contact hypersensitivity models; cytokine measurement Journal of immunology Medium 18424708
2018 Treg-intrinsic CD83 expression is essential for Treg differentiation upon activation; conditional Treg-specific CD83 knockout mice develop a pro-inflammatory phenotype with loss of Treg-specific differentiation markers and induction of an inflammatory profile. Treg-specific conditional CD83 knockout mice; scRNA-seq; flow cytometry; autoimmunity models JCI insight Medium 29875316
2019 DC-specific conditional CD83 knockout DCs produce drastically increased IL-2, higher CD25 and OX40L expression, causing superior T cell responses and compromised Treg suppressive functions; CD83-deficient DCs express increased IL-12 after bacterial encounter, leading to accelerated immune responses and exacerbated autoimmunity in EAE. DC-specific CD83 conditional KO (CD83ΔDC) mice; bacterial infection models (Salmonella, Listeria); EAE model; flow cytometry; cytokine measurements JCI insight Medium 31527313
2016 B cell-specific CD83 knockout B cells show defective upregulation of MHC class II and CD86 after stimulation, impaired proliferation, a shift toward increased dark zone GC B cells, and enhanced IgE responses; CD83-deficient B cells have a competitive disadvantage in GC responses. B cell-specific CD83 conditional KO mice; mixed BM chimeras; GC analysis by flow cytometry; immunization experiments; Borrelia burgdorferi infection model Journal of immunology Medium 26983787
2011 Activated T cells induce CD83 expression on B cells through CD40 engagement (not TCR/MHC binding or soluble factors), as demonstrated by anti-CD40L antibody blockade and transwell experiments. T cell receptor transgenic mice; transwell co-culture; anti-CD40L antibody blockade; in vivo peptide injection; flow cytometry Immunology letters Medium 21277328
2004 Soluble CD83 treatment of mature DCs completely alters their cytoskeleton (assessed by phalloidin, tubulin, and fascin staining), causing cell rounding and loss of veils, and completely inhibits DC-T cell cluster formation. Phalloidin, tubulin, and fascin immunofluorescence staining; DC-T cell clustering assays; recombinant sCD83 treatment Immunobiology Low 15481147
2023 CD83 expression in murine microglia is associated with pro-resolving functions; conditional deletion of CD83 in microglia results in an over-activated state during EAE neuroinflammation, with increased recruitment of pathogenic immune cells to the CNS and exacerbated disease. Conditional microglia-specific CD83 KO mice; EAE model; single-cell RNA-sequencing; flow cytometry of CNS infiltrates Nature communications Medium 37528070
2014 Membrane CD83 on mature DCs enhances intracellular calcium release in T lymphocytes upon DC-T cell contact; CD83 knockdown or antibody blockade reduces calcium signal amplitude and T cell proliferation. siRNA knockdown of CD83; anti-CD83 antibody blockade; Fluo-4-AM calcium indicator; flow cytometry and confocal microscopy; CFSE proliferation assay; calcium chelation Journal of leukocyte biology Medium 24436459
2019 Soluble CD83 enhances resolution of antigen-induced arthritis by reducing IL-17A, IFN-γ, IL-6, TNF-α, and RANKL in joints; this mechanism is IDO-dependent (abrogated by 1-methyltryptophan) and also involves TGF-β (blocked by anti-TGF-β antibodies), with induction of regulatory T cells. Mouse AIA model; IDO inhibitor (1-methyltryptophan); anti-TGF-β antibody blockade; flow cytometry of Tregs; cytokine measurement; histological analysis of bone destruction Frontiers in immunology Medium 31001257

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 Human blood dendritic cells selectively express CD83, a member of the immunoglobulin superfamily. Journal of immunology (Baltimore, Md. : 1950) 640 7706722
2010 Immature immunosuppressive CD14+HLA-DR-/low cells in melanoma patients are Stat3hi and overexpress CD80, CD83, and DC-sign. Cancer research 330 20484028
1998 Prostaglandin E2 induces the final maturation of IL-12-deficient CD1a+CD83+ dendritic cells: the levels of IL-12 are determined during the final dendritic cell maturation and are resistant to further modulation. Journal of immunology (Baltimore, Md. : 1950) 245 9743339
2005 IL-18-induced CD83+CCR7+ NK helper cells. The Journal of experimental medicine 235 16203865
2002 CD83 on dendritic cells: more than just a marker for maturation. Trends in immunology 191 12072358
2011 CD83 increases MHC II and CD86 on dendritic cells by opposing IL-10-driven MARCH1-mediated ubiquitination and degradation. The Journal of experimental medicine 187 21220452
2002 CD83 expression influences CD4+ T cell development in the thymus. Cell 173 11955430
2007 CD83 expression on dendritic cells and T cells: correlation with effective immune responses. European journal of immunology 168 17301951
2000 Human decidua contains potent immunostimulatory CD83(+) dendritic cells. The American journal of pathology 144 10880386
2005 CD83 is preformed inside monocytes, macrophages and dendritic cells, but it is only stably expressed on activated dendritic cells. The Biochemical journal 141 15320871
2005 Engagement of CD83 ligand induces prolonged expansion of CD8+ T cells and preferential enrichment for antigen specificity. Blood 139 16239433
2019 CD83: Activation Marker for Antigen Presenting Cells and Its Therapeutic Potential. Frontiers in immunology 138 31231400
2004 Infection of mature monocyte-derived dendritic cells with human cytomegalovirus inhibits stimulation of T-cell proliferation via the release of soluble CD83. Blood 122 14962896
2008 Rheumatoid arthritis synovium contains two subsets of CD83-DC-LAMP- dendritic cells with distinct cytokine profiles. The American journal of pathology 120 18292234
2007 CD83: an update on functions and prospects of the maturation marker of dendritic cells. Archives of dermatological research 120 17334966
2004 Prevention and treatment of experimental autoimmune encephalomyelitis by soluble CD83. The Journal of experimental medicine 116 15289503
2000 Expression of CCR6 and CD83 by cytokine-activated human neutrophils. Blood 114 11090084
2001 A soluble form of CD83 is released from activated dendritic cells and B lymphocytes, and is detectable in normal human sera. International immunology 113 11431426
2020 The CD83 Molecule - An Important Immune Checkpoint. Frontiers in immunology 109 32362900
1999 HLA-G in the human thymus: a subpopulation of medullary epithelial but not CD83(+) dendritic cells expresses HLA-G as a membrane-bound and soluble protein. International immunology 108 10360962
2008 CD83 regulates lymphocyte maturation, activation and homeostasis. Trends in immunology 98 18329338
2007 CD83 knockdown in monocyte-derived dendritic cells by small interfering RNA leads to a diminished T cell stimulation. Journal of immunology (Baltimore, Md. : 1950) 98 17442926
2002 Cutting edge: CD83 regulates the development of cellular immunity. Journal of immunology (Baltimore, Md. : 1950) 90 11884422
2005 TGF-beta and vitamin D3 utilize distinct pathways to suppress IL-12 production and modulate rapid differentiation of human monocytes into CD83+ dendritic cells. Journal of immunology (Baltimore, Md. : 1950) 84 15699136
2001 CD83 is an I-type lectin adhesion receptor that binds monocytes and a subset of activated CD8+ T cells [corrected]. Journal of immunology (Baltimore, Md. : 1950) 83 11238630
2016 CD83 Modulates B Cell Activation and Germinal Center Responses. Journal of immunology (Baltimore, Md. : 1950) 79 26983787
2001 Transdifferentiation of polymorphonuclear neutrophils: acquisition of CD83 and other functional characteristics of dendritic cells. Journal of molecular medicine (Berlin, Germany) 73 11511977
2002 Role of CD83 in the immunomodulation of dendritic cells. International archives of allergy and immunology 69 12403928
2007 Herpes simplex virus type 1 induces CD83 degradation in mature dendritic cells with immediate-early kinetics via the cellular proteasome. Journal of virology 68 17428858
2016 Thymic CD4 T cell selection requires attenuation of March8-mediated MHCII turnover in cortical epithelial cells through CD83. The Journal of experimental medicine 66 27503071
2006 Expression of CD83 is regulated by HuR via a novel cis-active coding region RNA element. The Journal of biological chemistry 66 16484227
2008 CD83 expression in CD4+ T cells modulates inflammation and autoimmunity. Journal of immunology (Baltimore, Md. : 1950) 64 18424708
2004 CD83(+)dendritic cells in the decidua of women with recurrent miscarriage and normal pregnancy. Placenta 64 14972446
2004 Homologs of CD83 from elasmobranch and teleost fish. Journal of immunology (Baltimore, Md. : 1950) 64 15383588
2009 Antibody to the dendritic cell surface activation antigen CD83 prevents acute graft-versus-host disease. The Journal of experimental medicine 61 19171763
2001 Human monocyte-derived and CD83(+) blood dendritic cells enhance NK cell-mediated cytotoxicity. European journal of immunology 60 11536161
2017 Soluble CD83 Inhibits T Cell Activation by Binding to the TLR4/MD-2 Complex on CD14+ Monocytes. Journal of immunology (Baltimore, Md. : 1950) 56 28193829
2004 The soluble form of CD83 is present at elevated levels in a number of hematological malignancies. Leukemia research 56 14687618
2010 Immunosuppression involving soluble CD83 induces tolerogenic dendritic cells that prevent cardiac allograft rejection. Transplantation 54 20861805
2006 Analysis of nucleocytoplasmic trafficking of the HuR ligand APRIL and its influence on CD83 expression. The Journal of biological chemistry 53 17178712
2001 Calcium signaling inhibits interleukin-12 production and activates CD83(+) dendritic cells that induce Th2 cell development. Blood 52 11588047
2005 Alternative splicing generates putative soluble CD83 proteins that inhibit T cell proliferation. Journal of immunology (Baltimore, Md. : 1950) 51 15905506
2018 CD83 expression is essential for Treg cell differentiation and stability. JCI insight 50 29875316
2007 CD83 is a regulator of murine B cell function in vivo. European journal of immunology 49 17266176
2007 Dendritic cell CD83: a therapeutic target or innocent bystander? Immunology letters 47 18001846
1997 In vitro generation of CD83+ human blood dendritic cells for active tumor immunotherapy. Experimental hematology 46 9091299
2007 A limited course of soluble CD83 delays acute cellular rejection of MHC-mismatched mouse skin allografts. Transplant international : official journal of the European Society for Organ Transplantation 45 17291220
2006 Melanogenesis and evidence for melanosome transport to the plasma membrane in a CD83 teleost leukocyte cell line. Pigment cell research 45 16704455
2007 CD83 modulates B cell function in vitro: increased IL-10 and reduced Ig secretion by CD83Tg B cells. PloS one 43 17710154
2020 Human CD83-targeted chimeric antigen receptor T cells prevent and treat graft-versus-host disease. The Journal of clinical investigation 42 32437331
2015 L Particles Transmit Viral Proteins from Herpes Simplex Virus 1-Infected Mature Dendritic Cells to Uninfected Bystander Cells, Inducing CD83 Downmodulation. Journal of virology 41 26311871
2008 CD83+CCR7- dendritic cells accumulate in the subepithelial dome and internalize translocated Escherichia coli HB101 in the Peyer's patches of ileal Crohn's disease. The American journal of pathology 41 19095953
1997 Hodgkin's cells express CD83, a dendritic cell lineage associated antigen. Pathology 41 9271021
2009 Decreased small airway and alveolar CD83+ dendritic cells in COPD. Chest 40 19465512
2005 CD83 monocyte-derived dendritic cells are present in human decidua and progesterone induces their differentiation in vitro. American journal of reproductive immunology (New York, N.Y. : 1989) 40 15760381
2004 A novel mutation in CD83 results in the development of a unique population of CD4+ T cells. Journal of immunology (Baltimore, Md. : 1950) 40 15322158
2001 Diverse functional activity of CD83+ monocyte-derived dendritic cells and the implications for cancer vaccines. Critical reviews in immunology 40 11642602
2014 Dendritic cell CD83 homotypic interactions regulate inflammation and promote mucosal homeostasis. Mucosal immunology 39 25204675
2011 CD83-stimulated monocytes suppress T-cell immune responses through production of prostaglandin E2. Proceedings of the National Academy of Sciences of the United States of America 39 22065790
2010 Prevention of chronic renal allograft rejection by soluble CD83. Transplantation 38 21079552
2009 The transmembrane E3 ligase GRAIL ubiquitinates and degrades CD83 on CD4 T cells. Journal of immunology (Baltimore, Md. : 1950) 37 19542455
2003 Latent membrane protein 1 of Epstein-Barr virus induces CD83 by the NF-kappaB signaling pathway. Journal of virology 37 12857898
2023 Microglial expression of CD83 governs cellular activation and restrains neuroinflammation in experimental autoimmune encephalomyelitis. Nature communications 36 37528070
2015 An immunohistochemical study of CD83- and CD1a-positive dendritic cells in the decidua of women with recurrent spontaneous abortion. European journal of medical research 36 25563385
2021 Eubacterium rectale Attenuates HSV-1 Induced Systemic Inflammation in Mice by Inhibiting CD83. Frontiers in immunology 35 34531862
2019 CD83 orchestrates immunity toward self and non-self in dendritic cells. JCI insight 35 31527313
2007 Unique features and distribution of the chicken CD83+ cell. Journal of immunology (Baltimore, Md. : 1950) 35 17911597
2004 Melanoma cells transfected to express CD83 induce antitumor immunity that can be increased by also engaging CD137. Proceedings of the National Academy of Sciences of the United States of America 35 15051893
2004 The soluble form of CD83 dramatically changes the cytoskeleton of dendritic cells. Immunobiology 35 15481147
2002 Cloning and characterization of the promoter region of the human CD83 gene. Immunobiology 34 12182451
2001 Detection of anaphylatoxin receptors on CD83+ dendritic cells derived from human skin. Immunology 34 11412308
2005 Upregulation of CD40, CD80, CD83 or CD86 on alveolar macrophages after lung transplantation. The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation 33 16102442
2014 Murine CD83-positive T cells mediate suppressor functions in vitro and in vivo. Immunobiology 32 25151500
2005 CD83 is a dimer: Comparative analysis of monomeric and dimeric isoforms. Biochemical and biophysical research communications 32 15721284
2003 Enhanced activation of CD83-positive T cells. Scandinavian journal of immunology 32 12950676
2016 The Analysis of CD83 Expression on Human Immune Cells Identifies a Unique CD83+-Activated T Cell Population. Journal of immunology (Baltimore, Md. : 1950) 31 27837105
2002 Overexpression, purification, and biochemical characterization of the extracellular human CD83 domain and generation of monoclonal antibodies. Protein expression and purification 31 11922761
2008 Induction of CD83+CD14+ nondendritic antigen-presenting cells by exposure of monocytes to IFN-alpha. Journal of immunology (Baltimore, Md. : 1950) 30 18713970
2019 Soluble CD83 Triggers Resolution of Arthritis and Sustained Inflammation Control in IDO Dependent Manner. Frontiers in immunology 28 31001257
2014 Herpes simplex virus type 1 ICP0 induces CD83 degradation in mature dendritic cells independent of its E3 ubiquitin ligase function. The Journal of general virology 28 24643878
2015 CD83 is required for the induction of protective immunity by a DNA vaccine in a teleost model. Developmental and comparative immunology 27 25800093
2015 Immunosuppressive human anti-CD83 monoclonal antibody depletion of activated dendritic cells in transplantation. Leukemia 27 26286117
2011 Activated T cells induce rapid CD83 expression on B cells by engagement of CD40. Immunology letters 27 21277328
1998 Low CD83, but normal MHC class II and costimulatory molecule expression, on spleen dendritic cells from HIV+ patients. AIDS research and human retroviruses 27 9566553
2014 Dendritic cell membrane CD83 enhances immune responses by boosting intracellular calcium release in T lymphocytes. Journal of leukocyte biology 26 24436459
2005 Comparative analysis of CD1a, S-100, CD83, and CD11c human dendritic cells in normal, premalignant, and malignant tissues. Histology and histopathology 26 16136499
2018 CD83 is a new potential biomarker and therapeutic target for Hodgkin lymphoma. Haematologica 25 29351987
2023 CD83 Regulates the Immune Responses in Inflammatory Disorders. International journal of molecular sciences 24 36769151
2013 Soluble human CD83 ameliorates lupus in NZB/W F1 mice. Immunobiology 24 23886695
2009 Engagement of CD83 on B cells modulates B cell function in vivo. Journal of immunology (Baltimore, Md. : 1950) 24 19234177
2015 CD1a+ and CD83+ Langerhans cells are reduced in lower lip squamous cell carcinoma. Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology 23 26661374
2010 Expression of Scophthalmus maximus CD83 correlates with bacterial infection and antigen stimulation. Fish & shellfish immunology 23 20561589
2002 In situ localization of CD83-positive dendritic cells in psoriatic lesions. Dermatology (Basel, Switzerland) 22 11937733
2000 CD83+ human dendritic cells transfected with tumor peptide cDNA by electroporation induce specific T-cell responses: A potential tool for gene immunotherapy. Cancer gene therapy 22 10811479
2023 High temperature inhibits vascular development via the PIF4-miR166-HB15 module in Arabidopsis. Current biology : CB 20 37442138
2022 Tilting the Balance: Therapeutic Prospects of CD83 as a Checkpoint Molecule Controlling Resolution of Inflammation. International journal of molecular sciences 20 35054916
2007 Soluble CD14 and CD83 from human neonatal antigen-presenting cells are inducible by commensal bacteria and suppress allergen-induced human neonatal Th2 differentiation. Infection and immunity 20 17526743
2017 Expression of soluble CD83 in plasma from early-stage rheumatoid arthritis patients is not modified by anti-TNF-α therapy. Cytokine 19 28267648
2015 Triple costimulation via CD80, 4-1BB, and CD83 ligand elicits the long-term growth of Vγ9Vδ2 T cells in low levels of IL-2. Journal of leukocyte biology 18 26561569
2006 Transgenic expression of a CD83-immunoglobulin fusion protein impairs the development of immune-competent CD4-positive T cells. European journal of immunology 18 16841299