Dendritic cell CD83: A therapeutic target or innocent bystander?

Prazma, Charlene M.; Tedder, Thomas F.

doi:10.1016/j.imlet.2007.10.001

Cited by 53 publications

(42 citation statements)

References 48 publications

(121 reference statements)

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“…Unlike CD36 and CD44, CD83 expression is usually restricted to a population of activated dendritic cells. Its specific role and ligands remain a matter of debate (Breloer and Fleischer, 2008;Prazma and Tedder, 2008).…”

Section: Immune Surface Molecules and Brain Circuitrymentioning

confidence: 99%

Neuronal expression of Cd36, Cd44, and Cd83 antigen transcripts maps to distinct and specific murine brain circuits

Glezer

Bittencourt

Rivest

2009

J of Comparative Neurology

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Cells recruited by the innate immune response rely on surface-expressed molecules in order to receive signals from the local environment and to perform phagocytosis, cell adhesion, and others processes linked to host defense. Hundreds of surface antigens designated through a cluster of differentiation (CD) number have been used to identify particular populations of leukocytes. Surprisingly, we verified that the genes that encode Cd36 and Cd83 are constitutively expressed in specific neuronal cells. For instance, Cd36 mRNA is expressed in some regions related to circuitry involved in pheromone responses and reproductive behavior. Cd44 expression, reanalyzed and detailed here, is associated with the laminar formation and midline thalamic nuclei in addition to striatum, extended amygdala, and a few hypothalamic, cortical, and hippocampal regions. A systemic immune challenge was able to increase Cd44 expression quickly in the area postrema and motor nucleus of the vagus but not in regions presenting expressive constitutive expression. In contrast to Cd36 and Cd44, Cd83 message was widely distributed from the olfactory bulb to the brain stem reticular formation, sparing the striatopallidum, olivary region, and cerebellum. Its pattern of expression nevertheless remained strongly associated with hypothalamic, thalamic, and hindbrain nuclei. Unlike the other transcripts, Cd83 mRNA was rapidly modulated by restraint stress. Our results indicate that these molecules might play a role in specific neural circuits and present functions other than those attributed to leukocyte biology. The data also suggest that these surface proteins, or their associated mRNA, could be used to label neurons in specific circuits/regions.

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Section: Immune Surface Molecules and Brain Circuitrymentioning

confidence: 99%

Neuronal expression of Cd36, Cd44, and Cd83 antigen transcripts maps to distinct and specific murine brain circuits

Glezer

Bittencourt

Rivest

2009

J of Comparative Neurology

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“…The transmembrane form of CD83 is expressed on mature dendritic cells (DCs), B cells, macrophages, activated T cells and T regulatory cells, and thymic epithelial cells (3,4). The expression on DCs is involved in the activation of T cell-mediated immune responses (5)(6)(7)(8); however, a soluble form of CD83, generated by splice variants or by shedding, inhibits T cell proliferation (9).…”

mentioning

confidence: 99%

Soluble CD83 Inhibits T Cell Activation by Binding to the TLR4/MD-2 Complex on CD14+ Monocytes

Horvatinovich

Grogan

Norris

et al. 2017

The Journal of Immunology

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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 PGE2 in a COX-2–dependent manner. sCD83 inhibited T cell proliferation, blocked IL-2 secretion, and rendered T cells unresponsive to further downstream differentiation signals mediated by IL-2. Therefore, we propose the tolerogenic mechanism of action of sCD83 to be dependent on initial interaction with APCs, altering early cytokine signal pathways and leading to T cell unresponsiveness.

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“…The CD83 is a surface marker that distinguishes immature and mature human dendritic cell populations (Prazma and Tedder, 2008). The CD83 is type 1 glycoprotein belonging to the immunoglobulin superfamily and has been known to be one of the best markers for characterization of cultured DCs.…”

Section: Discussionmentioning

confidence: 99%

Effect of Dexamethasone on Phenotyping of Dendritic Cells: In vitro and in vivo Study

Al-Ashmawy¹,

El-Zamaran²,

El-Ashmawy³

et al. 2015

Science, Technology and Development

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Background: Glucocorticoids are known to suppress the immune response and are widely used as immunosuppressive agents in the treatment of many autoimmune and allergic diseases. Aim: This study investigated the effect of the steroid dexamethasone (DEX) on maturation and differentiation of DCs derived from monocytes. In addition, an in vivo experiment was conducted to investigate whether treatment of mice with DEX has immunomodulatory effect on murine splenic DCs. Methods: In vitro experiment: Immature DCs were generated by incubating peripheral blood monocytes with cytokine cocktail (GM-CSF+IL-4) for 9 days. Phenotypic analysis of the DCs' specific cell marker CD83 was performed by flow cytometry. In vivo experiment: Mice were randomly divided into 5 groups according to the dose of i.p., injection of DEX and duration of treatment. The murine splenic DCs were isolated and phenotyped for CD83 and CD11c by flow cytometry. Results: Addition of 1 µM DEX to the culture on day 7 or 8 resulted in a significant increase in the CD83 expression. The in vivo experiment showed that i.p. injection of DEX significantly increased the expression of CD83 on splenic DCs. Mice groups treated with a single dose of 20 mg kgG 1 DEX showed a significant decrease of percentage of CD11c + CD83 + splenic DCs. Conclusion: DEX induced the DCs to be more tolerogenic both in vitro and in vivo. It could be suggested that DEX can trigger immunosuppressive effect via modulating the expression of the cell surface markers of DCs.

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Dendritic cell CD83: A therapeutic target or innocent bystander?

Cited by 53 publications

References 48 publications

Neuronal expression of Cd36, Cd44, and Cd83 antigen transcripts maps to distinct and specific murine brain circuits

Neuronal expression of Cd36, Cd44, and Cd83 antigen transcripts maps to distinct and specific murine brain circuits

Soluble CD83 Inhibits T Cell Activation by Binding to the TLR4/MD-2 Complex on CD14+ Monocytes

Effect of Dexamethasone on Phenotyping of Dendritic Cells: In vitro and in vivo Study

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