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

Novak, Hermann; Müller, Anke; Harrer, Nathalie; Günther, Claudia; Carballido, José M.; Woisetschläger, Maximilian

doi:10.4049/jimmunol.178.7.4335

Cited by 45 publications

(30 citation statements)

References 48 publications

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“…Previous studies identified the STAT6, NFAT, NF-ĸB, and AP-1 binding sites in the 5′ flanking region of the CCL23 gene [13,14]. However, our results suggest that other transcription factor(s) may be involved in the transcriptional regulation of CCL23 because neither GM-CSF nor IL-5 activates those known transcription factors.…”

Section: Discussioncontrasting

confidence: 53%

Human Eosinophils Produce and Release a Novel Chemokine, CCL23, in vitro

Matsumoto

Fukuda

Hashimoto

et al. 2011

Int Arch Allergy Immunol

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Background: CCL23 (MPIF1/CK-BETA-8) is a novel CC chemokine that plays important roles in the inhibition of myeloid progenitor cell development, the selective recruitment of resting T lymphocytes and monocytes, and the potentiation of VEGF-induced proliferation and migration of human endothelial cells. Since eosinophils participate in the pathogenesis of airway remodeling, we examined CCL23 production and release by human eosinophils in vitro. Methods: Using Ficoll and antibody-coated immunomagnetic beads, eosinophils and other blood cells were purified from peripheral blood samples obtained from normal subjects and mildly allergic patients. Eosinophils were cultured in the presence of 10 ng/ml granulocyte-macrophage colony-stimulating factor (GM-CSF), 10 ng/ml IL-5, 100 ng/ml IFN-γ, 100 ng/ml IFN-α, or immobilized secretory IgA (sIgA). Total mRNA was extracted after 6 h of culture, and mRNA expression was measured using a microarray and RT-PCR. The CCL23 concentrations in the supernatants and cell lysates after 24 and 48 h of culture were measured by ELISA. Results: CCL23 mRNAs (both CK-β8-1 and CK-β8) were constitutively expressed in fresh eosinophils, and their expression levels were higher than in other types of blood cells. CCL23 mRNAs were significantly increased by stimulation with GM-CSF and IL-5 and slightly by IFN-α and immobilized sIgA. Fresh eosinophils contained trace amounts of CCL23 protein. CCL23 was significantly released into the supernatant when the eosinophils were stimulated with GM-CSF or IL-5 but not with IFN-γ or immobilized sIgA. Conclusion: Our data suggest that eosinophils produce and release CCL23 and may be involved in some in vivo physiological and pathological conditions.

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Section: Discussioncontrasting

confidence: 53%

Human Eosinophils Produce and Release a Novel Chemokine, CCL23, in vitro

Matsumoto

Fukuda

Hashimoto

et al. 2011

Int Arch Allergy Immunol

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“…While CCL23/MPIF-1 cDNA was originally isolated from a human aortic endothelial library (Patel et al, 1997), subsequent analysis made on various cell lines has shown that CCL23 mRNA is readily detectable in myelomonocytic cell lines (Patel et al, 1997). Expression of CCL23 mRNA was then found in monocytes stimulated with IL-1β (Forssmann et al, 1997) and it is now established that IL-4-treated monocytes produce remarkable amounts of CCL23 (Nardelli et al, 1999; Novak et al, 2007). CCL23 can be detected in synovial fluids from rheumatoid arthritis patients (Berahovich et al, 2005), as well as in serum of systemic sclerosis patients (Yanaba et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Human Neutrophils Produce CCL23 in Response to Various TLR-Agonists and TNFα

Arruda‐Silva

Bianchetto-Aguilera

Gasperini

et al. 2017

Front. Cell. Infect. Microbiol.

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CCL23, also known as myeloid progenitor inhibitory factor (MPIF)-1, macrophage inflammatory protein (MIP)-3, or CKβ8, is a member of the CC chemokine subfamily exerting its effects via CCR1 binding. By doing so, CCL23 selectively recruits resting T lymphocytes and monocytes, inhibits proliferation of myeloid progenitor cells and promotes angiogenesis. Previously, we and other groups have reported that human neutrophils are able to produce chemokines upon appropriate activation, including CCR1-binding CCL2, CCL3, and CCL4. Herein, we demonstrate that human neutrophils display the capacity to also express and release CCL23 when stimulated by R848 and, to a lesser extent, by other pro-inflammatory agonists, including LPS, Pam3CSK4, and TNFα. Notably, we show that, on a per cell basis, R848-activated neutrophils produce higher levels of CCL23 than autologous CD14+-monocytes activated under similar experimental conditions. By contrast, we found that, unlike CD14+-monocytes, neutrophils do not produce CCL23 in response to IL-4, thus indicating that they express CCL23 in a stimulus-specific fashion. Finally, we show that the production of CCL23 by R848-stimulated neutrophils is negatively modulated by IFNα, which instead enhances that of CCL2. Together, data extend our knowledge on the chemokines potentially produced by neutrophils. The ability of human neutrophils to produce CCL23 further supports the notion on the neutrophil capacity of orchestrating the recruitment of different cell types to the inflamed sites, in turn contributing to the control of the immune response.

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“…Within this pathway, the gene most differentially expressed in BRIDGE WB and demonstrating strong replication in CAMP WB was CCL23 (Table 3), an IL4/signal transducer and activator of transcription 6-induced chemoattractant of dendritic cells (31,32). In GSE9988, CCL23 was preferentially up-regulated in LPS-treated monocytes.…”

Section: Novel Biologic Insights Into Asthma Controlmentioning

confidence: 99%

Gene Expression Profiling in Blood Provides Reproducible Molecular Insights into Asthma Control

Croteau‐Chonka¹,

Qiu²,

Martínez

et al. 2017

Am J Respir Crit Care Med

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Rationale: Maintaining optimal symptom control remains the primary objective of asthma treatment. Better understanding of the biologic underpinnings of asthma control may lead to the development of improved clinical and pharmaceutical approaches.Objectives: To identify molecular pathways and interrelated genes whose differential expression was associated with asthma control.Methods: We performed gene set enrichment analyses of asthma control in 1,170 adults with asthma, each with gene expression data derived from either whole blood (WB) or unstimulated CD4 1 T lymphocytes (CD4), and a self-reported asthma control score representing either the preceding 6 months (chronic) or 7 days (acute). Our study comprised a discovery WB cohort (n = 245, chronic) and three independent, nonoverlapping replication cohorts: a second WB set (n = 448, acute) and two CD4 sets (n = 300, chronic; n = 77, acute). Measurements and Main Results:In the WB discovery cohort, we found significant overrepresentation of genes associated with asthma control in 1,106 gene sets from the Molecular Signatures Database (false discovery rate, ,5%). Of these, 583 (53%) replicated in at least one replication cohort (false discovery rate, ,25%). Suboptimal control was associated with signatures of eosinophilic and granulocytic inflammatory signals, whereas optimal control signatures were enriched for immature lymphocytic patterns. These signatures included two related biologic processes related to activation by TREM-1 (triggering receptor expressed on myeloid cells 1) and lipopolysaccharide. Conclusions:Together, these results demonstrate the existence of specific, reproducible transcriptomic components in blood that vary with degree of asthma control and implicate a novel biologic target (TREM-1).

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

Cited by 45 publications

References 48 publications

Human Eosinophils Produce and Release a Novel Chemokine, CCL23, in vitro

Human Eosinophils Produce and Release a Novel Chemokine, CCL23, in vitro

Human Neutrophils Produce CCL23 in Response to Various TLR-Agonists and TNFα

Gene Expression Profiling in Blood Provides Reproducible Molecular Insights into Asthma Control

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