Affinage

CCL23

C-C motif chemokine 23 · UniProt P55773

Length
120 aa
Mass
13.4 kDa
Annotated
2026-04-28
46 papers in source corpus 21 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CCL23 is a monomeric CC chemokine that functions as a pleiotropic mediator of leukocyte recruitment, angiogenesis, and immune regulation through signaling primarily via CCR1 and, via proteolytic processing of its alternatively spliced isoform, through FPRL1. Full-length CCL23 contains a unique 32-amino-acid N-terminal extension that is cleaved by matrix metalloproteinases to generate CCL23(26-99), a more potent CCR1 agonist, while inflammatory protease processing of the CKβ8-1 splice variant releases the SHAAGtide peptide, a high-potency FPRL1 agonist for monocyte and neutrophil recruitment (PMID:22147696, PMID:17513790). CCR1-mediated signaling proceeds through Gi/Go proteins to activate PLC, PKCδ, NF-κB, ERK1/2, and SAPK/JNK, driving monocyte chemotaxis, cell-cycle progression, endothelial migration, MMP-2 upregulation, and KDR/Flk-1-dependent potentiation of VEGF signaling in angiogenesis (PMID:9886417, PMID:19951712, PMID:15927850, PMID:19265684). CCL23 transcription in monocytes is induced by IL-4/IL-13 through a STAT6-dependent promoter element and by PMA through cooperative NFAT, NF-κB, and AP-1 sites, while in the tumor microenvironment macrophage-derived CCL23 promotes CD8+ T-cell exhaustion via GSK3β phosphorylation (PMID:17371990, PMID:17368823, PMID:35750747).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1999 High

    Identification of CCR1 as the specific receptor and delineation of the Gi-protein–PLC–PLA2 signaling cascade established the core signal transduction pathway underlying CCL23-driven monocyte chemotaxis.

    Evidence Radioligand competition binding, calcium flux in CCR1 transfectants and primary monocytes/DCs, pertussis toxin and PLC/PLA2 inhibitor studies

    PMID:9886417

    Open questions at the time
    • Downstream transcription factor targets of this cascade were not identified
    • Relative contributions of PLA2 vs PLC arms to chemotaxis not quantified
  2. 1999 High

    Genomic characterization revealed an atypical four-exon structure and recent duplication origin with HCC-2, while expression profiling showed constitutive CCL23 production by dendritic cells that is suppressed by IFN-γ and CD40 ligation, distinguishing its regulation from other CC chemokines.

    Evidence Genomic shotgun sequencing of 17q11.2 region; ELISA and Northern blot of monocyte-derived and CD34+-derived DCs with multiple stimuli

    PMID:10213461 PMID:10380905

    Open questions at the time
    • Functional significance of the fourth exon-encoded N-terminal extension was not yet known
    • Mechanism of CD40L-mediated suppression not defined
  3. 2000 High

    NMR structure determination showed CCL23 is a monomer with a canonical chemokine fold plus an extra disulfide bond and basic surface patches, providing a structural framework for understanding its extended N-terminus as a proprotein domain and its proteoglycan interactions.

    Evidence NMR solution structure with backbone dynamics analysis

    PMID:11060285

    Open questions at the time
    • Proteoglycan binding was inferred from surface charge but not directly measured
    • No co-crystal or NMR structure with CCR1
  4. 2005 High

    Discovery that CCL23 promotes angiogenesis—driving endothelial chemotaxis, tube formation, and in vivo neovascularization through CCR1, with an N-terminally truncated form 100-fold more potent—expanded its role from leukocyte chemoattractant to vascular biology effector.

    Evidence Transwell migration, tube formation, chick CAM neovascularization assay with pertussis toxin and anti-CCR1 blockade; structure-activity comparison of truncated vs full-length CCL23

    PMID:15927850

    Open questions at the time
    • Identity of the endogenous protease responsible for N-terminal truncation in vivo was unknown
    • Endothelial CCR1 expression levels in different vascular beds not characterized
  5. 2005 Medium

    CCL23 was shown to transcriptionally upregulate MMP-2 in endothelial cells and drive MMP-2-dependent Matrigel invasion, linking its angiogenic activity to extracellular matrix remodeling.

    Evidence MMP-2 promoter-reporter, RT-PCR, Western blot, Matrigel invasion with MMP inhibitors and neutralizing antibodies

    PMID:16378600

    Open questions at the time
    • Transcription factor mediating MMP-2 promoter activation by CCL23 not identified
    • No in vivo confirmation of MMP-2 dependence
  6. 2007 High

    Three convergent studies clarified CCL23 transcriptional regulation—STAT6-dependent IL-4/IL-13 induction in monocytes and NFAT/NF-κB/AP-1-dependent PMA induction—and revealed that proteolytic processing of the CKβ8-1 isoform releases SHAAGtide, a uniquely potent FPRL1 agonist for neutrophil and monocyte recruitment.

    Evidence Promoter mutagenesis/EMSA for STAT6 and NFAT/NF-κB/AP-1; protease incubation with MS-confirmed cleavage sites, calcium flux, Transwell migration, in vivo leukocyte recruitment

    PMID:17368823 PMID:17371990 PMID:17513790

    Open questions at the time
    • Relative in vivo contribution of FPRL1 vs CCR1 signaling during inflammation unknown
    • Nature of the downstream negative cis-element in the STAT6-regulated promoter not fully characterized
  7. 2009 Medium

    Detailed signaling pathway dissection established that CCL23 activates a Gi/Go → PLC → PKCδ → NF-κB cascade for chemotaxis and proinflammatory gene induction, while a parallel SAPK/JNK pathway mediates KDR/Flk-1 upregulation that potentiates VEGF-driven endothelial proliferation.

    Evidence Ordered pharmacological inhibitor studies in chemotaxis and NF-κB assays; KDR promoter-reporter and SAPK/JNK inhibitor studies with downstream ERK phosphorylation readout

    PMID:19265684 PMID:19951712

    Open questions at the time
    • Whether PKCδ and SAPK/JNK pathways branch from the same or distinct upstream nodes not resolved
    • In vivo relevance of KDR upregulation to CCL23-driven angiogenesis not tested
  8. 2010 Medium

    CCL23 was found to drive cell-cycle progression by upregulating cyclins D3 and B1 plus immediate-early genes c-Myc and Egr-1 via the Gi/Go → PLC → PKCδ → ERK1/2 pathway, extending its functional repertoire beyond chemotaxis to proliferative signaling.

    Evidence Cell cycle analysis, ERK1/2 phosphorylation, cyclin expression by Western blot, ordered inhibitor dissection

    PMID:20097574

    Open questions at the time
    • Cell type generality of cell-cycle effects not established beyond the model used
    • Direct link between ERK1/2 and cyclin D3/B1 transcription not demonstrated
  9. 2011 High

    A systematic MMP processing screen identified MMPs as the proteases that cleave the extended N-terminus of full-length CCL23(1-99) to generate the more potent CCL23(26-99) agonist, uniquely demonstrating that MMP cleavage activates rather than inactivates a CC chemokine.

    Evidence Family-wide in vitro MMP screen, MALDI-TOF-MS cleavage site mapping, calcium flux and Transwell migration in CCR1 transfectants and THP-1 cells

    PMID:22147696

    Open questions at the time
    • Which specific MMP family members are the physiological activators in vivo remains unclear
    • Structural basis for enhanced CCR1 agonism of CCL23(26-99) not determined
  10. 2017 Medium

    Neutrophils were identified as a significant cellular source of CCL23, particularly upon TLR7/8 stimulation, with IFNα serving as a negative modulator—broadening the producer cell repertoire beyond monocytes and dendritic cells.

    Evidence ELISA and RT-qPCR in purified primary neutrophils vs autologous monocytes with multiple TLR agonists and cytokines

    PMID:28553619

    Open questions at the time
    • Receptor and signaling pathway mediating TLR7/8-induced CCL23 transcription in neutrophils not mapped
    • In vivo contribution of neutrophil-derived CCL23 to inflammation not tested
  11. 2022 Medium

    In the tumor microenvironment, macrophage-derived CCL23 was shown to promote CD8+ T-cell exhaustion by upregulating CTLA-4, TIGIT, TIM-3, and LAG-3 through GSK3β phosphorylation, establishing a new immunomodulatory axis beyond chemotaxis.

    Evidence Phosphokinase array and Western blot for GSK3β in CD8+ T cells, flow cytometry for exhaustion markers, ELISA for CCL23 in ascites

    PMID:35750747

    Open questions at the time
    • Receptor on CD8+ T cells mediating GSK3β phosphorylation not identified (CCR1 vs other)
    • In vivo relevance to tumor immune evasion not confirmed by loss-of-function in animal models

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for enhanced CCR1 agonism of MMP-processed CCL23, the receptor mediating T-cell exhaustion effects, and the net in vivo balance between CCL23's pro-inflammatory leukocyte recruitment and immunosuppressive T-cell exhaustion functions in disease settings.
  • No CCL23–CCR1 co-structure available
  • No genetic loss-of-function model in mammals reported
  • Relative in vivo roles of CCR1 vs FPRL1 pathways not dissected

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 4 GO:0060089 molecular transducer activity 2
Localization
GO:0005576 extracellular region 4
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-168256 Immune System 5
Partners
CCR1ESR1FPRL1MMP2TFAP4

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 CCL23 (MPIF-1) binds specifically to CCR1 on monocytes and dendritic cells, competing with MIP-1α but not MIP-1β or MCP-1 for binding sites. Signal transduction proceeds through G proteins (pertussis toxin-sensitive), leading to phospholipase C activation, protein kinase C, calcium flux from both extracellular and intracellular pools, and phospholipase A2 activation, which is required for filamentous actin formation and chemotaxis. Radioligand competition binding ([125I]MIP-1α), calcium flux assays in CCR1-transfected HEK-293 cells and primary monocytes/DCs, GTP-γS inhibition, pertussis toxin pretreatment, PLC inhibitors, PLA2 inhibitors, [3H]arachidonic acid release assay Journal of immunology High 9886417
2000 CCL23 (MPIF-1) is a monomeric CC chemokine. NMR solution structure reveals a canonical chemokine fold (three β-strands and an overlying α-helix) plus two additional cysteines forming an extra disulfide bond beyond the conserved four. The extended N-terminus exists as a proprotein form; both full-length and truncated forms are monomers. The highly basic protein (pI >9) contains distinct positively charged pockets consistent with proteoglycan binding. NMR spectroscopy with backbone dynamics analysis The Journal of biological chemistry High 11060285
2000 CCL23 (CKβ-8) is chemotactic for human osteoclast precursors (TRAP-positive mononuclear cells from osteoclastoma tissue) at EC(max) of 0.1–0.3 nM, and this activity is partially cross-desensitized by RANTES and MIP-1α, implicating CCR1 as the mediating receptor. CCL23 had no chemotactic activity on osteoblasts. Chemotaxis assay with CCR1 cross-desensitization experiments; in situ hybridization for CCL23 mRNA in human fetal bone; immunolocalization of protein in osteophytic tissue Journal of cellular physiology Medium 10737895
1999 CCL23 (MPIF-1) is constitutively produced and released by monocyte-derived dendritic cells but not by macrophages or resting monocytes. CD40 ligation and IFN-γ treatment, unlike LPS or TNF-α, suppress MPIF-1 transcript and protein release from dendritic cells, indicating a distinct regulatory program compared to other CC/CXC chemokines. ELISA, Northern blot for MPIF-1 transcript, stimulation of monocyte-derived and CD34+-derived DCs with LPS, TNF-α, CD40L, IFN-γ Journal of leukocyte biology Medium 10380905
2005 CCL23 promotes chemotactic migration and tube formation of vascular endothelial cells and neovascularization in the chick chorioallantoic membrane via CCR1 (blocked by pertussis toxin or anti-CCR1 antibody). An N-terminally truncated form of CCL23 is at least 100-fold more potent than the intact form in angiogenic activity and comparable to FGF. Transwell chemotaxis assay, endothelial tube formation assay, chick chorioallantoic membrane neovascularization assay, pertussis toxin and antibody neutralization Cytokine High 15927850
2005 CCL23 enhances expression of MMP-2 (but not MMP-9, TIMP-1, TIMP-2, or MT1-MMP) in endothelial cells at the transcriptional level, and promotes endothelial cell invasion through Matrigel in an MMP-2-dependent manner (blocked by MMP inhibitors GM6001 and MMP-2 Inhibitor I, as well as anti-CCL23 and anti-CCR1 antibodies). RT-PCR, Western blot, MMP-2/Luc reporter gene assay, Matrigel invasion assay, neutralizing antibody blockade, MMP inhibitor studies Biochemical and biophysical research communications Medium 16378600
2007 Proinflammatory proteases cleave the alternatively spliced CCL23 isoform (CKβ8-1) immediately N-terminal to the 18-residue inserted domain, releasing a peptide termed SHAAGtide that acts as a potent FPRL1 (CCR12) agonist (50-100-fold more potent than other known FPRL1 ligands) and recruits monocytes and neutrophils in vitro and in vivo, while the remaining CCL23 body retains enhanced CCR1 activity. Sequential further cleavage within SHAAGtide abolishes FPRL1 activity. Protease incubation with synovial fluid and defined proteases, calcium flux assay, Transwell migration assay, in vivo leukocyte recruitment, MALDI-TOF-MS cleavage site mapping Journal of immunology High 17513790
2007 IL-4 and IL-13 induce CCL23 expression in human peripheral blood monocytes in a STAT6-dependent manner. A canonical STAT6 binding site in the CCL23 promoter is required for IL-4 responsiveness; mutation of this site abolishes induction, and two tandem copies confer responsiveness to a heterologous promoter. A downstream negative cis-element suppresses IL-4-induced CCL23 expression. Promoter reporter gene assays with STAT6 site mutagenesis, monocyte stimulation with IL-4/IL-13, EMSA, heterologous promoter constructs Journal of immunology High 17371990
2007 The CCL23 promoter region −293 to +31 is critical for PMA-induced expression in U937 monocytoid cells. Transcription factor binding sites at −269/−264 (NFAT), −167/−159 (NF-κB), and −51/−43 (AP-1) are each required for PMA-induced CCL23 expression, confirmed by factor binding and pathway-specific inhibitor studies. Serial deletion reporter analysis, EMSA for transcription factor binding, pharmacological signal pathway inhibitors Biochimica et biophysica acta Medium 17368823
2009 CCL23 (CKβ8) and its isoform CKβ8-1 induce chemotaxis and cell migration through a Gi/Go protein → PLC → PKCδ → NF-κB signaling pathway. Both isoforms activate NF-κB and increase mRNA expression of pro-inflammatory cytokines and adhesion molecules. CKβ8 and CKβ8-1 mRNA levels are elevated in foam cells, implicating CCL23 in atherosclerosis-related inflammation. Transwell chemotaxis assay with pharmacological inhibitors (Gi/Go, PLC, PKCδ, NF-κB), NF-κB activation assays, RT-PCR for inflammatory mediators in foam cells Life sciences Medium 19951712
2009 CCL23 up-regulates KDR/Flk-1 (VEGFR2) mRNA and protein expression in endothelial cells primarily at the transcriptional level, mediated through SAPK/JNK phosphorylation. CCL23-induced KDR/Flk-1 up-regulation potentiates VEGF-induced ERK phosphorylation and enhances VEGF-driven endothelial proliferation and migration. PCR, Western blot, confocal microscopy, KDR/Flk-1 reporter assay, SAPK/JNK inhibitor, ERK phosphorylation assay, proliferation and migration assays Biochemical and biophysical research communications Medium 19265684
2010 CCL23 (CKβ8) and CKβ8-1 induce cell-cycle progression and up-regulate cyclin D3 and cyclin B1 as well as immediate early genes c-Myc and Egr-1 through a Gi/Go protein → PLC → PKCδ → ERK1/2 cascade. Cell cycle analysis, ERK1/2 phosphorylation assay, pathway inhibitor studies (Gi/Go, PLC, PKCδ), cyclin expression by Western blot Cytokine Medium 20097574
2011 Matrix metalloproteinases (MMPs) cleave full-length CCL23(1-99) within its unique 32-amino acid extended N-terminus, generating CCL23(26-99) as the principal product. Unlike most CC chemokines where MMP cleavage inactivates, MMP-processed CCL23(26-99) is a stronger agonist in calcium flux assays and Transwell migration assays of CCR1-transfected cells and THP-1 monocytes compared to full-length CCL23. Cleavage sites were identified by MALDI-TOF-MS. Family-wide MMP processing screen, MALDI-TOF-MS cleavage site sequencing, calcium flux assay, Transwell migration assay in CCR1 transfectants and THP-1 cells The Journal of biological chemistry High 22147696
2011 CCL23 stimulates chemotaxis of THP-1 monocytes, enhances expression of adhesion molecule CD11c, and promotes release of MMP-2 from monocytes. Proatherogenic stimuli (oxidized LDL, oxidative stress) markedly enhance CCL23 release from THP-1 macrophages. Chemotaxis assay, flow cytometry for CD11c, zymography for MMP-2, ELISA for CCL23 release, RT-PCR for CCL23 in atherosclerotic lesions Inflammation research Medium 21656154
2017 Human neutrophils produce and release CCL23 in response to TLR7/8 agonist R848 and, to a lesser extent, LPS, Pam3CSK4, and TNF-α, but not IL-4. On a per-cell basis, R848-activated neutrophils produce more CCL23 than autologous CD14+ monocytes. IFNα negatively modulates CCL23 production by R848-stimulated neutrophils. ELISA for CCL23 protein, RT-PCR/real-time PCR for mRNA, stimulation of purified primary neutrophils and autologous monocytes with multiple TLR agonists and cytokines Frontiers in cellular and infection microbiology Medium 28553619
2021 CCL23 expression in liver cancer cells is transcriptionally regulated by ESR1. Conversely, CCL23 suppresses AKT signaling, which promotes ESR1 expression, forming a feedback loop. CCL23 acting through CCR1 also recruits CD8+ T cell infiltration and inhibits cancer cell proliferation, stemness, and mobility in liver cancer. Bioinformatics screening, RNA-seq, co-immunoprecipitation, AKT pathway western blot, CD8+ T cell infiltration analysis, functional assays (proliferation, stemness, migration) with CCL23 overexpression/knockdown Cancer science Medium 34050704
2022 Macrophage-derived CCL23 induces upregulation of immune checkpoint proteins (CTLA-4, TIGIT, TIM-3, LAG-3) on CD8+ T cells, promoting T-cell exhaustion, via phosphorylation of GSK3β in CD8+ T cells. ELISA for CCL23 in ascites, flow cytometry for exhaustion markers, phosphokinase array, Western blot for GSK3β phosphorylation, in vitro CCL23 treatment of CD8+ T cells British journal of cancer Medium 35750747
2022 CCL23 interacts with transcription factor TFAP4 (demonstrated by co-immunoprecipitation), and overexpression of CCL23 inhibits HCC cell proliferation, invasion, and angiogenesis (tube formation, VEGFA/VEGFR expression) in vitro, while co-expression of TFAP4 blocks these CCL23-mediated inhibitory effects. Co-immunoprecipitation, overexpression plasmid transfection, proliferation assay, invasion assay, HUVEC tube formation assay, RT-qPCR and Western blot Bioengineered Medium 35001801
2023 CCL23 inhibits lung leukocyte recruitment in a primate cardiopulmonary bypass model by slowing bone marrow transit of PMNs and monocytes and suppressing their circulatory release and alveolar appearance, without suppressing CD11b/L-selectin expression or post-surgical cytokine levels in BALF. In vivo primate CPB model, BrdU labeling of BM-derived leukocytes, flow cytometry, bronchoalveolar lavage with cytokine ELISA; CCL23 given intravenously Heart, lung & circulation Medium 36628657
1999 The CCL23 gene (MPIF-1/SCYA23) is located on human chromosome 17q11.2, has four exons (unlike the three-exon structure of most CC chemokines), and shares high conservation with neighboring HCC-2 gene (SCYA15) including introns and flanking sequences, indicating recent gene duplication. Large-scale genomic sequencing (random shotgun), gene prediction, EST similarity search Journal of interferon & cytokine research High 10213461
2025 CCL23-stimulated THP-1 macrophages exhibit reduced CXCL10 secretion via STAT-3 activation, suggesting CCL23 modulates macrophage cytokine output in the tumor microenvironment. ELISA for CXCL10, in vitro CCL23 peptide stimulation of differentiated THP-1 monocytes, STAT-3 pathway analysis Cancers Low 41463176

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 Inducible expression of a CC chemokine liver- and activation-regulated chemokine (LARC)/macrophage inflammatory protein (MIP)-3 alpha/CCL20 by epidermal keratinocytes and its role in atopic dermatitis. International immunology 145 11133838
2008 Potential novel biomarkers of disease activity in rheumatoid arthritis patients: CXCL13, CCL23, transforming growth factor alpha, tumor necrosis factor receptor superfamily member 9, and macrophage colony-stimulating factor. Arthritis and rheumatism 112 18668547
2001 Selective recruitment of CCR6-expressing cells by increased production of MIP-3 alpha in rheumatoid arthritis. Clinical and experimental immunology 109 11472439
2000 The CC chemokine CK beta-11/MIP-3 beta/ELC/Exodus 3 mediates tumor rejection of murine breast cancer cells through NK cells. Journal of immunology (Baltimore, Md. : 1950) 102 10754294
2011 Increased expression of the chemokine CCL23 in eosinophilic chronic rhinosinusitis with nasal polyps. The Journal of allergy and clinical immunology 89 21497884
2005 Human CC chemokine CCL23, a ligand for CCR1, induces endothelial cell migration and promotes angiogenesis. Cytokine 84 15927850
2002 Expression of the C-C chemokine MIP-3 alpha/CCL20 in human epidermis with impaired permeability barrier function. Experimental dermatology 81 11994140
2006 Enhanced expression and clinical significance of CC-chemokine MIP-3 alpha in hepatocellular carcinoma. Scandinavian journal of immunology 60 16764701
2011 Biochemical analysis of matrix metalloproteinase activation of chemokines CCL15 and CCL23 and increased glycosaminoglycan binding of CCL16. The Journal of biological chemistry 58 22147696
1999 Characterization of the signal transduction pathway activated in human monocytes and dendritic cells by MPIF-1, a specific ligand for CC chemokine receptor 1. Journal of immunology (Baltimore, Md. : 1950) 58 9886417
2000 CKbeta-8 [CCL23], a novel CC chemokine, is chemotactic for human osteoclast precursors and is expressed in bone tissues. Journal of cellular physiology 57 10737895
2017 Human Neutrophils Produce CCL23 in Response to Various TLR-Agonists and TNFα. Frontiers in cellular and infection microbiology 54 28553619
2005 Human CC chemokine CCL23 enhances expression of matrix metalloproteinase-2 and invasion of vascular endothelial cells. Biochemical and biophysical research communications 44 16378600
2018 CCL23: a new CC chemokine involved in human brain damage. Journal of internal medicine 43 29415332
2007 Effects of MIP-1 alpha, MIP-3 alpha, and MIP-3 beta on the induction of HIV Gag-specific immune response with DNA vaccines. Molecular therapy : the journal of the American Society of Gene Therapy 42 17356539
2022 Macrophage-derived CCL23 upregulates expression of T-cell exhaustion markers in ovarian cancer. British journal of cancer 41 35750747
2007 CCL23 expression is induced by IL-4 in a STAT6-dependent fashion. Journal of immunology (Baltimore, Md. : 1950) 38 17371990
2011 Potential involvement of CCL23 in atherosclerotic lesion formation/progression by the enhancement of chemotaxis, adhesion molecule expression, and MMP-2 release from monocytes. Inflammation research : official journal of the European Histamine Research Society ... [et al.] 36 21656154
2020 CCL23: A Chemokine Associated with Progression from Mild Cognitive Impairment to Alzheimer's Disease. Journal of Alzheimer's disease : JAD 32 31958084
1999 Organization of the chemokine gene cluster on human chromosome 17q11.2 containing the genes for CC chemokine MPIF-1, HCC-2, HCC-1, LEC, and RANTES. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 31 10213461
2021 CCL23 suppresses liver cancer progression through the CCR1/AKT/ESR1 feedback loop. Cancer science 28 34050704
2006 Effect of oestradiol on PAMP-mediated CCL20/MIP-3 alpha production by mouse uterine epithelial cells in culture. Immunology 28 16771853
2000 Solution structure and dynamics of myeloid progenitor inhibitory factor-1 (MPIF-1), a novel monomeric CC chemokine. The Journal of biological chemistry 28 11060285
2009 CCL23 up-regulates expression of KDR/Flk-1 and potentiates VEGF-induced proliferation and migration of human endothelial cells. Biochemical and biophysical research communications 27 19265684
2009 CK beta 8/CCL23 induces cell migration via the Gi/Go protein/PLC/PKC delta/NF-kappa B and is involved in inflammatory responses. Life sciences 27 19951712
2004 Determinants of high-affinity binding and receptor activation in the N-terminus of CCL-19 (MIP-3 beta). Biochemistry 24 15035637
1999 Dendritic cells and MPIF-1: chemotactic activity and inhibition of endogenous chemokine production by IFN-gamma and CD40 ligation. Journal of leukocyte biology 24 10380905
2007 Proinflammatory proteases liberate a discrete high-affinity functional FPRL1 (CCR12) ligand from CCL23. Journal of immunology (Baltimore, Md. : 1950) 23 17513790
2011 Human eosinophils produce and release a novel chemokine, CCL23, in vitro. International archives of allergy and immunology 17 21646793
2014 Effect of diabetes and oxidative stress on plasma CCL23 levels in patients with severe chronic kidney disease. Polskie Archiwum Medycyny Wewnetrznej 12 24995525
2016 Clinical Severity and Tear Biomarkers, Eosinophil Cationic Protein and CCL23, in Chronic Allergic Conjunctival Diseases. Seminars in ophthalmology 11 27929738
2010 CKbeta8/CCL23 and its isoform CKbeta8-1 induce up-regulation of cyclins via the G(i)/G(o) protein/PLC/PKCdelta/ERK leading to cell-cycle progression. Cytokine 11 20097574
2023 Proteomic and transcriptomic screening demonstrates increased mast cell-derived CCL23 in systemic mastocytosis. The Journal of allergy and clinical immunology 10 36813186
2021 CCL23 in Balancing the Act of Endoplasmic Reticulum Stress and Antitumor Immunity in Hepatocellular Carcinoma. Frontiers in oncology 9 34671553
2014 CCL20/MIP-3 alpha mRNA expression in the conjunctival epithelium of normal individuals and patients with vernal keratoconjunctivitis. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie 8 25172034
2022 Inhibitory effect of CC chemokine ligand 23 (CCL23)/ transcription factor activating enhancer binding protein 4 (TFAP4) on cell proliferation, invasion and angiogenesis in hepatocellular carcinoma. Bioengineered 7 35001801
2007 Promoter analysis of human CC chemokine CCL23 gene in U937 monocytoid cells. Biochimica et biophysica acta 6 17368823
2024 Delayed CCL23 response is associated with poor outcomes after cardiac arrest. Cytokine 2 38325139
2007 [Effect of CCL23/myeloid progenitor inhibitory factor 1 (MPIF-1) on the proliferation, apoptosis and differentiation of U937 cells]. Zhongguo shi yan xue ye xue za zhi 2 17605852
2025 ARTN and CCL23 predicted chemosensitivity in acute myeloid leukemia: an Olink® proteomics approach. Clinical proteomics 1 39833682
2025 UCN expresses differently in left-sided and right-sided colon cancer contributing to distinct immune microenvironment via regulating CCL23. Human immunology 1 40274491
2026 Exploration and Validation of the Diagnostic Potential of the Circadian Rhythm-Related Genes CCL23 and VNN1 in Adolescents with Depressive Disorder. Molecular neurobiology 0 41706232
2026 Protective Causal Effects of CCL19, CCL23, and IL17A on Achilles Tendinitis: Insights from Bidirectional Mendelian Randomization and Metabolite-Mediated Pathway Analysis. Orthopedic research and reviews 0 41926501
2025 MIP-3-Alpha and MIP-3-Beta as Early Predictors of Pneumonia in Polytraumatized Patients. Lung 0 40074940
2025 Ovarian Cancer Ascites Enriched for CCL23 Reduces Macrophage-Derived CXCL10 Secretion and Is Associated with Poor Patient Outcomes. Cancers 0 41463176
2023 Myeloid Progenitor Inhibitory Factor-1 (CCL23) Inhibits Lung Leukocyte Recruitment in a Primate Cardiopulmonary Bypass-Induced Pulmonary Ischaemia Model. Heart, lung & circulation 0 36628657