Dendritic cells and MPIF-1: chemotactic activity and inhibition of endogenous chemokine production by IFN-γ and CD40 ligation

Nardelli, Bernardetta; Morahan, Diana K.; Bong, Gary W.; Semenuk, Mark; Kreider, Brent L.; Garotta, Gianni

doi:10.1002/jlb.65.6.822

Cited by 23 publications

(14 citation statements)

References 43 publications

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“…2, B and D). CCL23 is reported to be constitutively produced by MDDC and its expression down-regulated by inflammatory mediators (35) as is demonstrated in our transcript analysis. Expression of CCL15 by DC has not been previously reported but, intriguingly, this chemokine has high protein homology and functional similarities with CCL23 (36), suggesting some redundancy of function.…”

Section: Discussionsupporting

confidence: 75%

Human Immature Monocyte-Derived Dendritic Cells Express the G Protein-Coupled Receptor GPR105 (KIAA0001, P2Y14) and Increase Intracellular Calcium in Response to its Agonist, Uridine Diphosphoglucose

Skelton

Cooper²,

Murphy

et al. 2003

The Journal of Immunology

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Dendritic cells (DC) are essential to the initiation of an immune response due to their unique ability to take-up and process Ag, translocate to lymph nodes, and present processed Ag to naive T cells. Many chemokines, chemokine receptors and other G protein-coupled receptors (GPCRs) are implicated in these various aspects of DC biology. Through microarray analysis, we compared expression levels of chemokines, their cognate receptors, and selected GPCRs in human monocytes and in vitro monocyte-derived immature and mature DC. Hierarchical clustering of gene expression clearly distinguishes the three cell types, most notably highlighting exceptional levels of expression of the GPCR GPR105 within the immature monocyte-derived DC (MDDC) gene cluster. Little or no expression was observed within the monocyte and mature MDDC cluster. Putative functionality of the GPR105 receptor was demonstrated by an observed calcium flux in immature MDDC treated with the potent GPR105 agonist, uridine 5′-diphosphoglucose (UDP-glucose), while no response to the nucleotide sugar was seen in monocytes and mature MDDC. This UDP-glucose-induced calcium response was, at least in part, pertussis toxin-sensitive. Moreover, immature MDDC from some donors treated with UDP-glucose exhibit an increase in expression of the costimulatory molecule CD86, which correlates with the intensity of the UDP-glucose-induced calcium flux. Together, these data demonstrate differential expression of GPR105 on immature and mature MDDC and suggest a role for the receptor and its agonist ligand in DC activation.

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Section: Discussionsupporting

confidence: 75%

Human Immature Monocyte-Derived Dendritic Cells Express the G Protein-Coupled Receptor GPR105 (KIAA0001, P2Y14) and Increase Intracellular Calcium in Response to its Agonist, Uridine Diphosphoglucose

Skelton

Cooper²,

Murphy

et al. 2003

The Journal of Immunology

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“…DC have been shown to express CCL23 (15). Because these cells can be generated from monocytes by IL-4 and GM-CSF, it was determined whether CCL23 production was regulated in monocytes during the differentiation process into DC.…”

Section: Resultsmentioning

confidence: 99%

“…Maturation of monocyte-derived DC with agonistic CD40 Abs or IFN-␥ reduces CCL23 RNA and protein expression. In contrast, treatment of immature DC with IL-10 induces CCL23 production (15).…”

mentioning

confidence: 95%

“…An amino-terminally truncated form of CCL23 is also expressed which can also bind to formyl peptidereceptor-like 1 receptor (13). Functionally, CCL23 has chemotactic activity for monocytes (12,14), DC (15,16), lymphocytes, neutrophils (11), osteoclast precursor cells (17), and endothelial cells (18). In contrast, CCL23 reduces the proliferation of progenitor cells giving rise to granulocyte and monocyte lineages (11), whereas it enhances angiogenesis of endothelial cells (18).…”

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confidence: 99%

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CCL23 Expression Is Induced by IL-4 in a STAT6-Dependent Fashion

Novak

Müller

Harrer

et al. 2007

The Journal of Immunology

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The chemokine CCL23 is primarily expressed in cells of the myeloid lineage but little information about its regulation is available. In this study, it is demonstrated that IL-4 and IL-13 induced CCL23 expression in human peripheral blood monocytes. GM-CSF had no effect on its own but synergized with IL-4, but not IL-13. CCL23 promoter reporter gene constructs were sensitive to IL-4 stimulation in the presence of the transcription factor STAT6. A canonical STAT6 binding site in the promoter region of the CCL23 gene was critical for the IL-4-inducible phenotype because reporter plasmids with a defective STAT6 binding site were unable to respond to IL-4 stimulation. In addition, two tandem copies of the STAT6 site conferred cytokine responsiveness to a heterologous minimal promoter. Furthermore, IL-4 inducibility of the CCL23 promoter was dependent on the absence of a negatively acting cis-element downstream of the STAT6 binding site. The negative function of this element was operative also on heterologous IL-4-inducible promoters. CCL23 was also expressed in skin from patients suffering from atopic dermatitis at higher levels than in normal individuals. However, no correlation between CCL23 expression in the serum and IgE levels as a diagnostic marker for atopy was found. Collectively, these data suggest a link between the inducible phenotype of CCL23 expression in monocytes by the prototype Th2 molecule pair IL-4/STAT6 and the increased number of CCL23-expressing cells in skin of atopic dermatitis patients.

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“…Previous reports have suggested that CKβ8 transduces a signal through CCR1 belonging to the G protein-coupled receptor (Nardelli et al 1999;Patel et al 1997;Youn et al 1998). However, the associated downstream intracellular signaling pathway is not yet fully elucidated.…”

Section: Resultsmentioning

confidence: 96%

CKβ8/CCL23 induces cell migration via the Gi/Go protein/PLC/PKCδ/NF-κB and is involved in inflammatory responses

Kim

2010

Life Sciences

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Dendritic cells and MPIF-1: chemotactic activity and inhibition of endogenous chemokine production by IFN-γ and CD40 ligation

Cited by 23 publications

References 43 publications

Human Immature Monocyte-Derived Dendritic Cells Express the G Protein-Coupled Receptor GPR105 (KIAA0001, P2Y14) and Increase Intracellular Calcium in Response to its Agonist, Uridine Diphosphoglucose

Human Immature Monocyte-Derived Dendritic Cells Express the G Protein-Coupled Receptor GPR105 (KIAA0001, P2Y14) and Increase Intracellular Calcium in Response to its Agonist, Uridine Diphosphoglucose

CCL23 Expression Is Induced by IL-4 in a STAT6-Dependent Fashion

CKβ8/CCL23 induces cell migration via the Gi/Go protein/PLC/PKCδ/NF-κB and is involved in inflammatory responses

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