Disease relevance of CD83

• In two-thirds of the donors, R5- and X4-tropic HIV-1 strains induced partial up-regulation of DC activation markers such as CD83 and CD86 [1].
• We observed that DCs undergo full maturation in response to Salmonella infection, as indicated by up-regulation of cell-surface marker proteins CD80, CD83, CD86, and human leukocyte antigen class II [2].
• Infection studies with herpes simplex virus type 1 (HSV-1) and the inhibition of the CD83 mRNA specific transport from the nucleus to the cytoplasm suggested a possible functional role for CD83 [3].
• Upregulation of co-stimulatory molecule expression and dendritic cell marker (CD83) on B cells in periodontal disease [4].
• Significant upregulation of CD86 and CD83 expression was detected in periodontitis lesions, and most of this occurred on B cells [4].

Psychiatry related information on CD83

• The high frequency of the lupus-derived 16/6 Id in PBC may accompany the polyclonal B-cell activation seen in that disease [5].

High impact information on CD83

• This complex reduces the threshold for B cell activation via the B cell receptor by bridging Ag specific recognition and CD21-mediated complement recognition [6].
• Finally, we present evidence demonstrating that B cell activation via TI stimuli does not play merely a permissive role in allowing for cell cycle entry and enhanced responsiveness to other stimuli [7].
• A direct signal through binding of antigen to membrane Ig can enhance B cell antigen presentation and T-dependent B cell activation, but is not required for a productive interaction between a small resting B cell and a differentiated helper T cell [8].
• Among these secondary phenomena are decreased cytotoxic lymphocyte responses, polyclonal B-cell activation, decreased monocyte chemotaxis, and a number of serologic abnormalities [9].
• The extracellular cysteine-rich domain of the TNF-R is homologous to the nerve growth factor receptor and the B cell activation protein Bp50 [10].

Chemical compound and disease context of CD83

• Since the cell surface molecule CD83, a member of the immunoglobulin superfamily and a marker for mature dendritic cells, appeared on the surface of ER/EB2-5 cells within 3 h after the addition of estrogen, we analyzed the regulation of CD83 induction by EBV in more detail [11].
• In surgically resected, paraffin-embedded tissue sections from 70 patients with colorectal liver metastasis, CD83 (a marker of mature DCs) positive cells and cancer cells positive for the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assay were counted [12].
• Whereas CD83 expression was increased and IL-10 production was induced by Bifidobacterium bifidum, Bifidobacterium longum, and Bifidobacterium pseudocatenulatum, B. infantis failed to produce these effects [13].
• The transmembrane glycoprotein K1, encoded by the first open reading frame of KSHV, is a signaling protein capable of eliciting B-cell activation [14].
• Initial studies demonstrated that monocyte (M phi)-mediated suppression of the generation of ISC in Staphylococcus aureus (SA)-stimulated cultures was mitigated by indomethacin, and thus suggested that the cyclooxygenase pathway products of arachidonic acid played a role in the regulation of B cell activation [15].

Biological context of CD83

• Blood CD83+ cells had a cellular morphology characteristic of dendritic cells and a cell surface phenotype that did not correlate with that of T cells, B cells, NK cells, or cells of the myelomonocytic lineage [16].
• Furthermore, we showed that native CD83 is glycosylated and that this glycosylation influences the binding of the antibodies in Western blot analyses [17].
• After culture, cells from 24 samples exhibited morphological and immunophenotypic features of DCs, including expression of major histocompatibility complex class II, CD1a, CD83, and CD86, and were potent stimulators in an allogeneic mixed lymphocyte reaction (MLR) [18].
• The induction of CD83 and beta-chemokines was tyrosine phosphorylation dependent [19].
• In addition, SLE patients displayed selective down-regulation of the maturation marker CD83 and had abnormal responses to maturation stimuli [20].

Anatomical context of CD83

• Human blood dendritic cells selectively express CD83, a member of the immunoglobulin superfamily [16].
• CD83+ cells were also the most potent stimulator cells in an allogeneic MLR when compared with other leukocyte lineages [16].
• Immature moDC but not mature moDC nor monocytes captured CpG-ODNs. moDC stimulation with the CpG-A ODN D19 up-regulated CD83, CD86, and HLA-DR [21].
• We found two distinct populations of DC present in CD patients: a DC-specific ICAM-3 grabbing non-integrin (DC-SIGN)(+) population that was present scattered throughout the mucosa, and a CD83(+) population that was present in aggregated lymphoid nodules and as single cells in the lamina propria [22].
• Cultured cells had the morphological appearance of DC and expressed the DC-associated antigens CD1A (range 2-87%) and CD83 (15-44%) [23].

Associations of CD83 with chemical compounds

• Incubation of DCs with A23187 calcium ionophore for 48 h induced an expression of mature DC markers CD83 and fascin [24].
• In this study, analysis of leukocyte subpopulations isolated from human blood revealed that circulating or cultured B and T cells, NK cells, and monocytes did not express CD83, whereas CD83+ cells were predominantly found in the dendritic cell-enriched metrizamide low density fraction of plastic nonadherent blood mononuclear cells [16].
• When challenged by lipopolysaccharide, these cells upregulate costimulatory molecules, express CD83, and become mature DC [25].
• CD83 is a 45-kDa glycoprotein and member of the immunoglobulin (Ig) superfamily [17].
• From concentration-dependent changes in CD83 expression, we found an apparent ID50 >>1.5 micromol/L sulfasalazine [26].

Physical interactions of CD83

• Receptor binding studies with 125I-TNF-alpha demonstrate a marked increase in TNF-alpha binding sites after B cell activation (approximately 6,000 sites per cell, with an apparent Kd of 2.0 X 10(-10) M) [27].
• These findings indicate that CD21 ligands binding to the C3dg/EBV-binding site of CD21 markedly augment B cell activation initiated by Ag receptor ligation via a selective, c-fos-dependent signaling pathway [28].
• We induced maturation by the addition of TNF-alpha, IL-1beta, IL-6 and prostaglandin E2 to the medium and assessed cell maturity by the levels of the secreted p40 subunit of IL-12 and of membrane-bound CD83 [29].
• Freshly isolated or cultured dermal CD1a+ and CD83+ DC bound anti-C5aR and anti-C3aR monoclonal antibodies (mAbs), as detected by flow cytometry [30].
• The T-BAM/CD40-L molecule on CD4+ T cells interacts with B cell CD40 molecules to deliver contact-dependent signals that drive B cell activation and Ig secretion [31].

Enzymatic interactions of CD83

• Co-crosslinking of CD19 and BCR was shown to enhance B-cell activation due to the recruitment of further signaling molecules to the activator complex by the phosphorylated tyrosine residues of CD19 [32].

Regulatory relationships of CD83

• CD38 is expressed on human mature monocyte-derived dendritic cells and is functionally involved in CD83 expression and IL-12 induction [33].
• Stimulation of activated IL-4-Mo-DC through OX40L strikingly enhanced their maturation as evidenced by CD83 up-regulation, CD115 (CSF-1R) down-regulation, and typical morphologic changes [34].
• Among these neuropeptides, only VIP induces the production of bioactive IL-12 and the neoexpression of CD83 on a fraction of the DC population, with an effect significant at 100 and 10 nM, respectively [35].
• TNF-alpha induced the cluster formation of the cells and the enhancement of cell surface expression levels of CD83, CD86, and HLA-DR, and T cell stimulatory capacity, whereas the capacities for the endocytosis and the chemotactic migration were suppressed in these cells [36].
• In tonsil, FK-positive DC expressed CD83, a marker for mature DC [37].

Other interactions of CD83

• Following enrichment, DC developed an activated phenotype with up-regulation of CD80, CD86, and CD83 expression [38].
• CD83 expression was increased by a soluble factor secreted from BCG-CWS-treated DC and was completely inhibited by monoclonal antibodies against TNF-alpha [39].
• RESULTS: DCs cultured in FEP or PS had comparable cell yield, viability, and CD83 and CCR7 expression [40].
• However, both the early and the late HCMV conditioning medium, harvested from MRC-5 cells at 24 h or 7-9 days after infection, respectively, induced a higher ratio of DCs expressing maturation markers (CD40, CD83, CD86 and HLA-DR) on the surface of the cells [41].
• In normal colon the number of DC-SIGN(+) DC was lower and CD83(+) DC were detected only in very few solitary lymphoid nodules [22].

Analytical, diagnostic and therapeutic context of CD83

• In this study, we analyzed the expression of co-stimulatory molecules (CD80 and CD86) and CD83, which is a marker of mature dendritic cells, on gingival cells that were isolated from severe periodontitis tissues, with the use of flow cytometry [4].
• In vitro peripheral blood mononuclear cell cultures showed that stimulation with different periodontopathic bacteria, that included Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia, and Actinomyces viscosus, upregulated both CD86 and CD83 expression on B cells [4].
• Using these antibodies, CD83 was specifically recognized in FACS and Western blot analyses [17].
• Indirect immunofluorescence revealed CD83 inside immature DCs in perinuclear regions [42].
• Immunohistochemical studies of KSHV PCR+ MM BMSCs demonstrate expression of dendritic cell (DC) lineage markers (CD68, CD83, and fascin) [43].

References