Affinage

CCL24

C-C motif chemokine 24 · UniProt O00175

Length
119 aa
Mass
13.1 kDa
Annotated
2026-04-28
97 papers in source corpus 34 papers cited in narrative 34 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CCL24 (eotaxin-2) is a CC chemokine that signals exclusively through the Gi protein-coupled receptor CCR3 to orchestrate eosinophil recruitment, activation, and tissue remodeling across multiple organ systems. CCL24 binding to CCR3 activates ERK1/2, p38 MAPK, and PI3K cascades to drive eosinophil chemotaxis, actin polymerization, integrin switching, degranulation, and reactive oxygen species production, and additionally induces MUC5AC mucin expression in airway epithelial cells (PMID:9182688, PMID:9692884, PMID:12034562, PMID:12784909, PMID:37552963). CCL24 expression is regulated by IL-4/IL-13 via STAT6 in epithelial cells and macrophages, by GATA-1 in eosinophilic lineage cells, and by mechanotransduction through Piezo1-Wnt2/Wnt11 signaling in fibroblasts, with cell differentiation state determining production levels (PMID:11067944, PMID:15647285, PMID:17917245, PMID:38267432). Beyond eosinophil biology, CCL24 directly activates fibroblasts and stellate cells through CCR3-PI3K-TGF-β signaling to promote fibrosis in lung, liver, heart, skin, and peritoneum, drives M2 macrophage polarization, recruits immunosuppressive tumor-associated macrophages in colorectal and renal cancers, and stimulates trophoblast invasion via ERK1/2 and PI3K during placentation (PMID:32039405, PMID:40955564, PMID:36131165, PMID:41694595, PMID:26316550).

Mechanistic history

Synthesis pass · year-by-year structured walk · 23 steps
  1. 1997 High

    Identifying that the newly cloned eotaxin-2/CCL24 signals exclusively through CCR3 resolved the receptor specificity question for this chemokine and established it as an eosinophil and basophil chemoattractant with in vivo activity.

    Evidence Calcium mobilization, chemotaxis, mediator release, cross-desensitization with eotaxin/MCP-4, anti-CCR3 blocking antibody, and intradermal injection in rhesus monkeys

    PMID:9182688

    Open questions at the time
    • Intracellular signaling cascades downstream of CCR3 not yet mapped
    • Physiological sources of CCL24 in tissues unknown
    • Role beyond eosinophil/basophil recruitment uncharacterized
  2. 1998 High

    Demonstrating that CCL24-induced eosinophil actin polymerization and respiratory burst depend on pertussis toxin-sensitive Gi proteins established the G-protein coupling mechanism for CCR3 signaling.

    Evidence Pertussis toxin inhibition, anti-CCR3 antibody blocking, actin polymerization by flow cytometry, and ROS assay in primary eosinophils

    PMID:9692884

    Open questions at the time
    • Specific MAP kinase and lipid kinase cascades downstream of Gi not resolved
    • Whether CCL24 and eotaxin-1 activate identical downstream pathways through CCR3 not tested
  3. 2000 High

    Solving the NMR structure of CCL24 and mapping the CCR3 N-terminus binding groove revealed how CCL24 engages its receptor, and N-terminal truncation mutagenesis showed the amino terminus is essential for agonism and can be converted to antagonism.

    Evidence Heteronuclear NMR structure determination with 854 NOE restraints, receptor peptide chemical shift mapping, systematic N-terminal deletion mutants with calcium flux and chemotaxis assays

    PMID:10913244 PMID:11237428

    Open questions at the time
    • Full-length CCR3–CCL24 complex structure not available
    • Structural basis for the agonist-to-antagonist switch in truncated mutants unresolved
  4. 2000 High

    Establishing that IL-4-induced CCL24 expression in murine lung is STAT6-dependent identified the transcriptional pathway controlling CCL24 in allergic inflammation.

    Evidence STAT6-/- mice, IL-4 transgenic mice, Northern blot, and eosinophil chemotaxis with recombinant murine CCL24

    PMID:11067944

    Open questions at the time
    • Direct STAT6 binding to CCL24 promoter not shown at this stage
    • Tissue-specific transcriptional regulation (e.g. in gut vs lung) not resolved
  5. 2002 High

    Identifying ERK1/2 as the MAP kinase mediating CCL24-induced integrin switching from VLA-4/VCAM-1 to LFA-1/ICAM-1 revealed how CCR3 signaling controls eosinophil adhesion dynamics under physiologic shear.

    Evidence Parallel plate flow chamber, MEK inhibitor PD98059, CCR3-blocking antibody, adhesion molecule blocking antibodies

    PMID:12034562

    Open questions at the time
    • Whether additional kinases contribute to adhesion switching not tested
    • In vivo relevance of integrin switching for eosinophil tissue infiltration not demonstrated
  6. 2002 High

    Demonstrating that monocytes constitutively produce CCL24 while macrophages require IL-4 for induction revealed cell-state-dependent regulation and identified monocytes as a baseline source.

    Evidence Primary monocyte and monocyte-derived macrophage stimulation with LPS, IL-1β, IL-4, IL-13, TNF-α; ELISA and chemotaxis bioassay

    PMID:11823526

    Open questions at the time
    • Transcription factor(s) responsible for constitutive monocyte CCL24 expression not identified
    • Whether in vivo monocyte-derived CCL24 drives tissue eosinophilia not tested
  7. 2003 Medium

    Pharmacological dissection showing ERK1/2, p38 MAPK, and PI3K all contribute to CCR3-mediated eosinophil degranulation mapped the downstream signaling network for CCL24's effector functions.

    Evidence Specific kinase inhibitors (U0126, SB203580, LY294002) with eosinophil peroxidase degranulation assay in HL-60 eosinophilic cells

    PMID:12784909

    Open questions at the time
    • HL-60 cell line may not fully recapitulate primary eosinophil signaling
    • Relative contributions and hierarchy of the three kinase pathways not established
  8. 2005 High

    Using eotaxin-2 knockout mice to show that CCL24 is specifically required for airway luminal but not peribronchial eosinophilia, and that IL-13 is the essential inducer of CCL24 in airway macrophages, established compartment-specific, non-redundant functions for CCL24 versus eotaxin-1.

    Evidence IL-13-/- and eotaxin-2-/- mice, IL-13 transgenic and intratracheal models, compartment-specific cell and chemokine analysis

    PMID:15647285

    Open questions at the time
    • Whether CCL24 deficiency affects chronic airway remodeling not assessed
    • Redundancy with CCL26/eotaxin-3 not tested in this context
  9. 2006 Medium

    Showing that CCL24 directly stimulates fibroblast proliferation and collagen synthesis extended its biological role beyond immune cell recruitment to stromal cell activation and tissue fibrosis.

    Evidence 3H-thymidine proliferation, 3H-hydroxyproline collagen assay, α-SMA staining in primary human lung fibroblasts

    PMID:20143648

    Open questions at the time
    • Receptor (CCR3) involvement on fibroblasts not explicitly confirmed in this study
    • In vivo fibrotic contribution not tested at this stage
  10. 2007 Medium

    Loss- and gain-of-function experiments for GATA-1 in eosinophilic lineage cells identified GATA-1 as a transcription factor driving CCL24 production, adding a second regulatory pathway beyond STAT6.

    Evidence siRNA knockdown and overexpression of GATA-1 in ATRA-differentiated HT93 eosinophilic cells, CCL24 ELISA

    PMID:17917245

    Open questions at the time
    • Direct GATA-1 binding to CCL24 promoter not demonstrated
    • In vivo contribution of GATA-1-driven CCL24 not tested
  11. 2013 Medium

    Demonstrating that CCL24 promotes extravillous trophoblast migration, invasion, MMP2 activation, and ECM adhesion extended CCL24's functional repertoire to reproductive biology and placentation.

    Evidence Matrigel invasion, wound healing, zymography, ECM adhesion assay in HTR8/SVneo trophoblast cells

    PMID:23477905

    Open questions at the time
    • In vivo relevance in placentation not established
    • Whether CCR3 mediates trophoblast effects not confirmed in this study
  12. 2015 Medium

    Establishing that CCL24 activates trophoblast proliferation and invasion specifically through CCR3-ERK1/2 and PI3K (not JNK or p38) confirmed the receptor and refined the signaling pathway in this reproductive context.

    Evidence Pathway-specific inhibitors for ERK1/2, PI3K, JNK, p38; Western blot; proliferation and invasion assays in trophoblast cells

    PMID:26316550

    Open questions at the time
    • In vivo placental phenotype of CCL24 deficiency unknown
    • Whether CCL24 is essential for spiral artery remodeling not tested
  13. 2015 High

    Identifying CD163 on alveolar macrophages as a negative regulator of CCL24 production and showing that anti-CCL24 antibody reverses CD163-deficiency-driven eosinophilia and mucous metaplasia established a macrophage-intrinsic checkpoint for CCL24.

    Evidence Cd163-/- mice, anti-CCL24 neutralizing antibody, adoptive macrophage transfer, HDM/Der p1 allergen challenge

    PMID:26376364

    Open questions at the time
    • Signaling mechanism from CD163 engagement to CCL24 suppression not defined
    • Human relevance not confirmed
  14. 2016 High

    Finding that TPL-2/MAP3K8 in dendritic cells negatively regulates CCL24 expression, and that DC-derived CCL24 drives exaggerated airway eosinophilia, identified a second immune-cell-intrinsic kinase checkpoint governing CCL24 output.

    Evidence Map3k8-/- mice, conditional DC-specific KO, bone marrow chimeras, adoptive transfer, anti-CCL24 blockade, RNA-seq

    PMID:27484038

    Open questions at the time
    • Direct targets of TPL-2 that suppress CCL24 transcription not identified
    • Whether TPL-2 regulation of CCL24 operates in human DCs untested
  15. 2019 High

    Demonstrating that anti-CCL24 antibody CM-101 blocks fibroblast-to-myofibroblast transition and reduces bleomycin-induced dermal and pulmonary fibrosis provided proof-of-concept that CCL24 neutralization is a viable anti-fibrotic therapeutic strategy.

    Evidence CM-101 anti-CCL24 mAb, primary fibroblast and endothelial activation assays with SSc serum, prevention and treatment bleomycin mouse models

    PMID:31129606

    Open questions at the time
    • Specific CCR3 downstream signaling in dermal fibroblasts not dissected
    • Long-term efficacy and human translation not yet established
  16. 2020 High

    Genetic knockout and antibody blockade across three liver injury models established CCL24 as a direct driver of hepatic stellate cell activation and liver fibrosis through CCR3, broadening CCL24's fibrotic role to the liver.

    Evidence Ccl24-/- mice, MCD/STAM/TAA models, CM-101 antibody, LX2 hepatic stellate cell motility and collagen secretion assays

    PMID:32039405

    Open questions at the time
    • Whether CCL24 acts on other liver cell types (cholangiocytes, hepatocytes) not addressed here
    • PI3K/TGF-β signaling axis in stellate cells not fully mapped at this point
  17. 2020 High

    Identifying a gankyrin-STAT3-CCL24 positive feedback loop in renal cell carcinoma, where STAT3 directly binds the CCL24 promoter, demonstrated a cancer-specific transcriptional mechanism and autocrine signaling circuit promoting tumor progression.

    Evidence Co-IP for gankyrin-STAT3, ChIP for STAT3 on CCL24 promoter, CCR3 inhibitor SB328437, subcutaneous/metastasis/orthotopic mouse models

    PMID:32051393

    Open questions at the time
    • Whether this loop operates in cancers beyond RCC not tested
    • Relationship between STAT3 and STAT6 regulation of CCL24 not reconciled
  18. 2022 Medium

    Demonstrating that CCL24 promotes M2 macrophage polarization and cardiac fibroblast activation in heart failure extended the CCL24-CCR3 fibrotic axis to the heart and added macrophage polarization as a CCL24-driven immune effect.

    Evidence Anti-CCL24 antibody, Ang II-induced cardiac hypertrophy model, single-cell CyTOF, RNA-seq, primary cardiac fibroblast assays

    PMID:36131165

    Open questions at the time
    • Specific intracellular signaling in macrophage polarization not dissected
    • Single lab; independent replication needed
  19. 2023 Medium

    Showing that CCL24 induces MUC5AC via CCR3-ERK1/2/p38 MAPK in airway epithelial cells added mucin hypersecretion as a direct epithelial consequence of CCL24 signaling, relevant to asthma and chronic rhinosinusitis.

    Evidence Kinase inhibitors and siRNA for ERK1/2 and p38, CCR3 inhibitor SB328437, NCI-H292 cells and primary nasal epithelial cells

    PMID:37552963

    Open questions at the time
    • In vivo confirmation of CCL24-driven mucin hypersecretion not provided
    • Contribution relative to other mucin-inducing stimuli unknown
  20. 2023 High

    Spatial transcriptomics and primary cell assays showing CCL24 promotes hepatic stellate cell and cholangiocyte proliferation in PSC models, with CM-101 reducing biliary fibrosis and cholestasis, extended the hepatic fibrosis mechanism to biliary disease and cholangiocyte biology.

    Evidence Mdr2-/- and ANIT models, CM-101 antibody, primary human HSC and cholangiocyte proliferation assays, spatial transcriptomics

    PMID:37345655

    Open questions at the time
    • Whether CCL24 signals through CCR3 on cholangiocytes specifically not confirmed
    • Human PSC clinical validation pending
  21. 2024 Medium

    Identification of Piezo1 as a mechanosensor driving CCL24 secretion via Wnt2/Wnt11 in fibroblasts on stiff substrates revealed a mechanotransduction pathway linking tissue stiffness to CCL24-mediated fibrosis amplification.

    Evidence Piezo1 siRNA and AAV knockdown, stiffness-controlled substrates, Wnt pathway analysis, mouse skin fibrosis model

    PMID:38267432

    Open questions at the time
    • Whether Piezo1-CCL24 axis operates in other fibrotic organs not tested
    • Direct link between Wnt2/Wnt11 and CCL24 transcription not mechanistically resolved
  22. 2025 High

    Fibroblast-specific CCR3 deletion and CCL24 global knockout converging on reduced cardiac fibrosis established that the CCL24-CCR3-PI3K-TGF-β axis in fibroblasts is the critical effector pathway in pressure-overload cardiac remodeling.

    Evidence CCL24 KO mice, fibroblast-specific CCR3 CRISPR/Cas9 KO, TAC model, PI3K inhibition, anti-CCL24 antibody, CCR3 antagonist

    PMID:40955564

    Open questions at the time
    • Whether macrophage-derived CCL24 is the sole relevant source in the heart not definitively shown
    • Downstream TGF-β isoform specificity not determined
  23. 2026 Medium

    Showing that tumor-derived CCL24 recruits CCR3+ TAMs that undergo YAP1 nuclear translocation to promote immunosuppression in CRC established CCL24 as a tumor immune evasion mechanism acting through Hippo pathway co-option in macrophages.

    Evidence CCL24 KO CRC cells, syngeneic and AOM/DSS models, macrophage/CD8+ T cell co-cultures, YAP1 nuclear translocation analysis

    PMID:41694595

    Open questions at the time
    • Whether YAP1 activation is CCR3-dependent not formally tested
    • Single lab; independent confirmation needed
    • Generalizability beyond CRC not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the full-length CCR3-CCL24 complex structure, the integration of multiple transcriptional regulators (STAT6, STAT3, GATA-1, KLF7) at the CCL24 promoter in different cell types, and whether therapeutic CCL24 blockade can be translated across fibrotic diseases in humans.
  • No full-length CCR3–CCL24 structural model exists
  • Unified promoter architecture integrating STAT6, STAT3, GATA-1, and KLF7 inputs not resolved
  • Clinical efficacy of CCL24 neutralization in human fibrotic diseases not yet established by the primary literature

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 8
Localization
GO:0005576 extracellular region 6
Pathway
R-HSA-168256 Immune System 8 R-HSA-162582 Signal Transduction 6 R-HSA-1474244 Extracellular matrix organization 5
Partners
CCR3GATA1PIEZO1STAT3STAT6

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 CCL24 (eotaxin-2) signals exclusively through CCR3 to induce chemotaxis of eosinophils and basophils, and stimulate histamine and leukotriene C4 release from IL-3-primed basophils; complete cross-desensitization with eotaxin and MCP-4 confirmed shared CCR3 usage, and an anti-CCR3 monoclonal antibody abrogated all functional responses. Calcium mobilization assay, chemotaxis assay, mediator release assay, receptor desensitization, anti-CCR3 blocking antibody, in vivo intradermal injection in rhesus monkey The Journal of experimental medicine High 9182688
1998 CCL24 activates eosinophil actin polymerization, chemotaxis, and reactive oxygen species (respiratory burst) release via CCR3 and pertussis toxin-sensitive Gi proteins; CCR3-blocking antibody inhibited Ca2+ mobilization and ROS release, demonstrating Gi protein-coupled CCR3 signaling. Actin polymerization (NBD-phallacidin/flow cytometry), ROS assay, pertussis toxin inhibition, anti-CCR3 monoclonal antibody (7B11) blocking, Ca2+ mobilization European journal of immunology High 9692884
2000 NMR solution structure of CCL24 was determined: a helical turn (residues 17-20), 3-stranded antiparallel beta-sheet, and C-terminal alpha-helix, with two conserved disulfide bonds tethering the N-terminus/N-loop to the beta-sheet. The N-terminal region of CCR3 binds into an extended groove at the interface between the N-loop and the beta2-beta3 hairpin of CCL24. Heteronuclear and triple resonance NMR; hybrid distance geometry-simulated annealing structure calculation from 854 NOE restraints; receptor N-terminal peptide binding by NMR chemical shift mapping Biochemistry High 10913244
2000 The amino terminus of CCL24 (MPIF-2) is critical for eosinophil activity: deletion of the first two amino acids does not markedly alter activity, but subsequent truncations abolish Ca2+ mobilization, chemotaxis, and receptor binding on eosinophils. One N-terminal mutant (P30-R99) was converted from agonist to antagonist of CCR3 on eosinophils while retaining ability to inhibit myeloid progenitor colony formation, demonstrating separable structure-activity relationships. N-terminal deletion mutagenesis, calcium flux assay, chemotaxis assay, receptor binding, myeloid progenitor colony inhibition assay Cytokine High 11237428
2000 Murine CCL24 (eotaxin-2) mRNA expression is highest constitutively in jejunum and spleen, is induced by allergen challenge and IL-4 overexpression in lung, and the IL-4-induced expression is STAT6-dependent (abrogated in STAT6-deficient mice). Recombinant murine CCL24 induced dose-dependent chemotaxis of murine eosinophils but not macrophages or neutrophils. Northern blot, mouse genetic knockouts (STAT6-/-), IL-4 transgenic mice, recombinant protein chemotaxis assay Journal of immunology High 11067944
2002 CCL24 acts via MAP kinases (ERK1/2) downstream of CCR3 to shift eosinophil integrin usage: CCL24 co-immobilized with adhesion molecules decreased VCAM-1-mediated adhesion and increased ICAM-1-mediated adhesion. This was blocked by a CCR3-blocking mAb and by the MEK inhibitor PD98059. Parallel plate flow system (physiologic shear stress), adhesion molecule blocking mAbs, CCR3-blocking mAb, MEK/ERK inhibitor (PD98059), video microscopy American journal of respiratory cell and molecular biology High 12034562
2002 Peripheral blood monocytes constitutively produce bioactive CCL24 protein; production is upregulated by IL-1beta, LPS, and zymosan but not by Th2 cytokines (IL-4, IL-13) or TNF-alpha. IL-4 suppresses LPS-induced CCL24 from monocytes. Upon differentiation into macrophages, constitutive CCL24 production is suppressed, but IL-4 (not LPS) upregulates CCL24 in macrophages, demonstrating cell-state-dependent regulation. ELISA for CCL24 protein, cytokine stimulation assays in primary monocytes and monocyte-derived macrophages, chemotaxis bioassay Journal of immunology High 11823526
2002 CCL24 stimulates eosinophil degranulation (eosinophil peroxidase release) and superoxide anion generation via CCR3; anti-CCR3 antibody inhibited these effector functions. IL-5 cooperates with CCL24 to potentiate eosinophil degranulation. Eosinophil peroxidase degranulation assay, superoxide generation assay, anti-CCR3 blocking antibody, IL-5 priming, HL-60 eosinophilic cells Experimental biology and medicine Medium 12192108
2003 CCL24-induced eosinophil degranulation is mediated through ERK1/2 (MEK1/2), p38 MAPK, and PI3K signaling downstream of CCR3; specific inhibitors (U0126, SB203580, LY294002) concentration-dependently reduced CCR3-mediated degranulation. Specific kinase inhibitors (U0126 for MEK1/2, SB203580 for p38, LY294002 for PI3K), eosinophil peroxidase degranulation assay, HL-60 eosinophilic cells Immunopharmacology and immunotoxicology Medium 12784909
2003 CCL24 backbone dynamics determined by 15N NMR relaxation: the N-loop and third beta-strand forming the receptor-binding groove show substantial mobility, suggesting conformational rearrangements during receptor binding; comparison with eotaxin and eotaxin-3 reveals conserved dynamic features at the putative CCR3-binding surface. 15N NMR relaxation (T1, T2, NOE measurements), model-free analysis of backbone dynamics Proteins High 12486712
2003 IL-4 and IL-13 upregulate CCL24 production by bronchial epithelial cells; IFN-gamma and glucocorticoids attenuate this production, demonstrating cytokine-dependent transcriptional regulation of CCL24 in the airway epithelium. In vitro bronchial epithelial cell stimulation, mRNA expression analysis, ELISA for CCL24 protein, immunohistochemistry in asthmatic biopsies Cellular immunology Medium 14698143
2005 IL-13 is required for allergen-induced CCL24 expression in the lung (eotaxin-2 mRNA almost completely absent in IL-13 gene-targeted mice after OVA challenge). In eotaxin-2 knockout mice, airway (luminal) eosinophilia after IL-13 administration is profoundly reduced, but peribronchial tissue eosinophilia is preserved. Macrophages in the airway lumen are the IL-13-induced source of CCL24, distinct from eotaxin-1 expressed in tissue. Gene-targeted mice (IL-13-/-, eotaxin-2-/-), IL-13 lung transgenic mice, intratracheal IL-13 administration, compartment-specific eosinophil and chemokine analysis, immunohistochemistry The Journal of biological chemistry High 15647285
2003 IL-13 directly stimulates oesophageal tissue (via STAT6 signaling) to produce CCL24 (and CCL11), and this oesophagus-derived CCL24 is sufficient to promote eosinophil migration; STAT6-deficient oesophageal rings fail to produce CCL24 upon IL-13 treatment. Isolated oesophageal ring ex vivo assay, STAT6-/- mice, ELISA, eosinophil chemotaxis assay Clinical and experimental allergy High 20030665
2006 CCL24 (but not CCL26/eotaxin-3) directly stimulates human lung fibroblast proliferation and collagen synthesis, demonstrating a direct profibrogenic role for CCL24 on stromal cells independent of eosinophil recruitment. 3H-thymidine proliferation assay, 3H-hydroxyproline collagen incorporation, biochemical staining, Boyden chamber chemotaxis, alpha-SMA immunostaining, TGF-beta1 ELISA Annals of allergy, asthma & immunology Medium 20143648
2006 Epithelial differentiation state determines CCL24 vs CCL26 production in response to IL-4/IL-13: squamous differentiated ALI cultures produce predominantly CCL24, while mucociliary differentiated cultures produce predominantly CCL26. TNF-alpha reduces IL-4-induced CCL24 in submerged but not ALI cultures. Air-liquid interface (ALI) culture with varying retinoic acid concentrations, submerged cultures, IL-4/IL-13 stimulation, mRNA and protein quantification Molecular immunology Medium 16740309
2007 CCL24 production by eosinophil-lineage cells is regulated by the transcription factor GATA-1: ATRA-induced differentiation of HT93 cells into eosinophilic lineage upregulates CCR3 and CCL24 production; siRNA knockdown of GATA-1 reduces differentiation markers and CCL24 production, while GATA-1 overexpression enhances CCL24 production. ATRA-induced differentiation, siRNA knockdown of GATA-1, GATA-1 overexpression clones, MACS-enriched CCR3+ cells, ELISA for CCL24 Biological & pharmaceutical bulletin Medium 17917245
2013 CCL24 stimulates migration, invasion, and adhesion of extravillous trophoblasts (HTR8/SVneo cells), increases MMP2 activity (without affecting TIMP2), and promotes binding to collagen IV and fibronectin, identifying a role for CCL24 in placental trophoblast invasion and spiral arteriole remodeling. xCELLigence real-time system, wound-healing assay, Matrigel invasion assay, zymography, reverse zymography, extracellular matrix adhesion assay, recombinant human CCL24 Human reproduction Medium 23477905
2015 CCL24 promotes trophoblast proliferation, viability, and invasiveness via CCR3 through ERK1/2 and PI3K signaling pathways (not JNK or p38), activating Ki67 and MMP9; steroid hormones (progesterone, hCG) and decidual stromal cells upregulate CCL24/CCR3 in trophoblasts. Recombinant CCL24, pathway inhibitors (ERK1/2, PI3K, JNK, p38), proliferation and invasion assays, Western blot for downstream molecules Reproduction Medium 26316550
2015 CD163 on alveolar macrophages binds Der p1 (house dust mite allergen) in a calcium-dependent manner; CD163 deficiency leads to augmented CCL24 production by macrophages in response to Der p1, which in turn drives airway eosinophilia and mucous cell metaplasia reversible by anti-CCL24 neutralizing antibody. Cd163-/- mice, HDM/Der p1 challenge model, anti-CCL24 neutralizing antibody, adoptive transfer of alveolar macrophages, BMMΦ stimulation, proteomic analysis of CD163-Der p1 binding Mucosal immunology High 26376364
2016 TPL-2 (MAP3K8) kinase in dendritic cells negatively regulates CCL24 expression; TPL-2-deficient (Map3k8-/-) mice show exaggerated airway eosinophilia upon HDM challenge that is dependent on elevated DC-derived CCL24, and blockade of CCL24 prevents the exaggerated eosinophilia in mice receiving HDM-pulsed Map3k8-/- DCs. Map3k8-/- mice, mixed bone marrow chimeras, conditional DC-specific KO, adoptive transfer, anti-CCL24 blockade, ELISA, RNA sequencing The Journal of allergy and clinical immunology High 27484038
2017 Commensal microbiota maintains alveolar macrophages at low CCL24 production; antibiotic-mediated depletion of commensal bacteria increases CCL24 secretion from alveolar macrophages, which suppresses γδT17 cell-mediated anti-tumor responses. Adoptive transfer of normal alveolar macrophages or CCL24 antibody neutralization restored γδT17 cells and anti-tumor activity. Antibiotic-treated mouse model, adoptive transfer of alveolar macrophages, CCL24 antibody neutralization, flow cytometry, gene expression analysis Scientific reports Medium 28785009
2019 CCL24 blockade with monoclonal antibody CM-101 significantly reduces activation of dermal fibroblasts, their transition to myofibroblasts induced by SSc serum, and inhibits endothelial cell activation; in bleomycin-induced animal models, CM-101 profoundly inhibited both dermal and pulmonary fibrosis and inflammation. Anti-CCL24 monoclonal antibody (CM-101), primary fibroblast and endothelial cell activation assays with SSc serum, bleomycin mouse models (prevention and treatment), histology Annals of the rheumatic diseases High 31129606
2020 CCL24 drives liver fibrosis and inflammation through CCR3: Ccl24 knockout mice show attenuated MCD-diet-induced liver damage; CM-101 anti-CCL24 antibody reduces liver fibrosis in three experimental models (MCD, STAM, TAA). Mechanistically, CCL24 promotes hepatic stellate cell (HSC) motility, alpha-SMA expression, and pro-collagen I secretion via CCR3. Ccl24 knockout mice, MCD/STAM/TAA animal models, anti-CCL24 antibody (CM-101), LX2 HSC activation assays (motility, alpha-SMA, pro-collagen I), liver histology and fibrosis scoring JHEP reports High 32039405
2020 In clear cell renal cell carcinoma, gankyrin recruits STAT3 via direct binding, and STAT3 binds the CCL24 promoter to drive CCL24 expression. Autocrine CCL24 then enhances gankyrin expression and STAT3 activation via CCR3, forming a positive regulatory loop that promotes tumor progression and pazopanib resistance. Co-IP (gankyrin-STAT3 interaction), ChIP assay (STAT3 binding to CCL24 promoter), CCR3 inhibitor (SB328437), gankyrin knockdown/overexpression, in vivo subcutaneous/metastasis/orthotopic models, antibody chip for secreted factors Cell death & disease High 32051393
2022 CCL24/CCR3 axis promotes M2 macrophage polarization and cardiac fibroblast activation in heart failure: CCR3 is expressed on macrophages and fibroblasts; CCL24 antibody reduces Ang II-induced cardiac hypertrophy, fibrosis, and M2 macrophage/monocyte polarization; in vitro, CCL24 promotes cardiac fibroblast activation and migration through CCR3's G protein-coupled receptor function. CCL24 antibody treatment, Ang II mouse model, single-cell CyTOF, RNA-seq, immunofluorescence co-localization, in vitro primary cardiac fibroblast activation assays Cell biology and toxicology Medium 36131165
2023 CCL24 promotes proliferation of primary human hepatic stellate cells and cholangiocytes; in Mdr2-/- PSC mice, CCL24 is expressed in liver macrophages; CM-101 (anti-CCL24) reduces biliary inflammation, fibrosis, and cholestasis markers. Spatial transcriptomics showed CCL24 neutralization reduced cholangiocyte proliferation and senescence. Mdr2-/- mouse model, anti-CCL24 antibody (CM-101), primary human HSC and cholangiocyte proliferation assays, spatial transcriptomics, ANIT cholestasis mouse model JCI insight High 37345655
2024 Increased matrix stiffness drives CCL24 secretion via the mechanosensitive ion channel Piezo1 through the Wnt2/Wnt11 signaling pathway; Piezo1 knockdown in dermal fibroblasts abolishes fibroproliferative phenotypes even on stiff substrates, and AAV-mediated Piezo1 knockdown ameliorates skin fibrosis progression in mice. Piezo1 knockdown (siRNA, AAV), Wnt2/Wnt11 pathway analysis, stiffness-controlled substrates, in vivo mouse skin fibrosis model, CCL24 ELISA Cell death & disease Medium 38267432
2023 CCL24 induces MUC5AC mucin expression in airway epithelial cells via CCR3-mediated ERK1/2 and p38 MAPK signaling; CCR3 inhibitor (SB328437) and specific ERK1/2 (U0126) and p38 (SB203580) inhibitors, as well as siRNA knockdown of ERK1/2 and p38, blocked CCL24-induced MUC5AC upregulation in NCI-H292 cells and primary nasal epithelial cells. RT-PCR, ELISA, Western blot, specific kinase inhibitors (U0126, SB203580, SB328437), ERK1/2 and p38 siRNA knockdown, primary human nasal epithelial cells International archives of allergy and immunology Medium 37552963
2025 Cardiac-resident macrophages are the primary source of CCL24 in the heart during pressure overload. CCL24 deficiency ameliorates cardiac fibrosis following transverse aortic constriction (TAC). CCL24 directly activates cardiac fibroblasts through CCR3 via PI3K signaling and TGF-beta release. Fibroblast-specific CCR3 deletion (CRISPR/Cas9) improves cardiac function and reduces fibrosis comparably to CCL24 deficiency. CCL24-blocking antibody or CCR3 antagonist both enhanced cardiac function in pressure-overloaded mice. CCL24 KO mice, TAC model, fibroblast-specific CCR3 CRISPR/Cas9 KO, primary cardiac fibroblast activation assays, PI3K inhibition, CCL24-blocking antibody, CCR3 antagonist, cardiac function measurements Circulation research High 40955564
2023 CCL24 intraperitoneal injection in mice selectively recruits neutrophils and monocytes; in PSC patients and CCL24-treated hepatic stellate cells, CCL24 activates monocyte and neutrophil chemotaxis pathways. CM-101 anti-CCL24 antibody in an ANIT-induced cholestasis mouse model inhibits peribiliary neutrophil and macrophage accumulation while reducing biliary hyperplasia and fibrosis. In vivo CCL24 injection with flow cytometry, anti-CCL24 antibody treatment in ANIT mouse model, serum proteomics (Olink assay), in vitro HSC treatment with CCL24 Cells Medium 38334601
2025 mTORC1 hyperactivation in fibroblasts and interstitial macrophages suppresses CCL24 expression via aberrant STAT3 signaling and promotes CCR3 expression in macrophages, forming a dysregulated CCL24-CCR3 axis that drives sarcoid-like granuloma formation; rapamycin and azithromycin attenuate granuloma burden and normalize CCL24-CCR3 signaling. TSC1/TSC2 conditional KO (Fsp1-Cre) mice, cytokine/chemokine array, rapamycin and azithromycin treatment, STAT3 signaling analysis bioRxivpreprint Medium 40791394
2026 CCL24 secreted by colorectal cancer tumor cells recruits CCR3+ tumor-associated macrophages (TAMs), which promote immunosuppression by driving nuclear translocation of YAP1 (Hippo pathway transcription factor); CCL24 knockout or antibody-mediated inhibition suppresses TAM accumulation, increases CD8+ T cells, and reduces tumor growth in immunocompetent but not immunodeficient mice. CCL24 knockout CRC cells, co-culture with macrophages/CD8+ T cells, subcutaneous and metastasis syngeneic mouse models, AOM/DSS CRC model, YAP1 nuclear translocation analysis, flow cytometry International journal of biological sciences Medium 41694595
2026 Macrophage-derived CCL24 promotes mesothelial-to-mesenchymal transition (MMT) via the CCR3/p38 MAPK pathway in peritoneal fibrosis; pMSC-derived exosomes deliver miR-320d into macrophages, which suppresses CCL24 synthesis via the KLF7/STAT3 pathway, thereby ameliorating MMT-driven peritoneal fibrosis. CRISPR-Cas9 CCL24 KO podocytes, miR-320d mimic/inhibitor, KLF7 target validation, STAT3 phosphorylation analysis, CCR3/p38 MAPK pathway inhibitors, pMSC-derived exosomes, rat peritoneal dialysis model Scientific reports Medium 41781517
2016 CCL24 increases TLR4 expression in human coronary artery endothelial cells via JNK/SAPK and p38 MAPK transcriptional signaling, and post-transcriptionally via RNA-binding proteins HuR and TTP stabilizing TLR4 mRNA, and PRAT4A-regulated TLR4 trafficking; in vivo, CCL24 administration worsened high-cholesterol diet-induced atherosclerosis in LdlrWT but not LdlrTlr4 mice, confirming TLR4 dependence. In vitro endothelial cell stimulation with CCL24, TLR4 siRNA, kinase inhibitors (JNK, p38, ERK1/2), HuR/TTP/PRAT4A pathway analysis, Ldlr/LdlrTlr4 mice with high-cholesterol diet American journal of translational research Medium 28078007

Source papers

Stage 0 corpus · 97 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 Eotaxin-2, a novel CC chemokine that is selective for the chemokine receptor CCR3, and acts like eotaxin on human eosinophil and basophil leukocytes. The Journal of experimental medicine 328 9182688
1999 Eosinophil chemotactic chemokines (eotaxin, eotaxin-2, RANTES, monocyte chemoattractant protein-3 (MCP-3), and MCP-4), and C-C chemokine receptor 3 expression in bronchial biopsies from atopic and nonatopic (Intrinsic) asthmatics. Journal of immunology (Baltimore, Md. : 1950) 312 10570327
2002 Eotaxin (CCL11) and eotaxin-2 (CCL24) induce recruitment of eosinophils, basophils, neutrophils, and macrophages as well as features of early- and late-phase allergic reactions following cutaneous injection in human atopic and nonatopic volunteers. Journal of immunology (Baltimore, Md. : 1950) 213 12193745
1999 C-C chemokines in allergen-induced late-phase cutaneous responses in atopic subjects: association of eotaxin with early 6-hour eosinophils, and of eotaxin-2 and monocyte chemoattractant protein-4 with the later 24-hour tissue eosinophilia, and relationship to basophils and other C-C chemokines (monocyte chemoattractant protein-3 and RANTES). Journal of immunology (Baltimore, Md. : 1950) 179 10491000
2000 Murine eotaxin-2: a constitutive eosinophil chemokine induced by allergen challenge and IL-4 overexpression. Journal of immunology (Baltimore, Md. : 1950) 127 11067944
2005 Identification of a cooperative mechanism involving interleukin-13 and eotaxin-2 in experimental allergic lung inflammation. The Journal of biological chemistry 126 15647285
2007 Coexpression of IL-5 and eotaxin-2 in mice creates an eosinophil-dependent model of respiratory inflammation with characteristics of severe asthma. Journal of immunology (Baltimore, Md. : 1950) 120 17548626
2003 Tear and mucus eotaxin-1 and eotaxin-2 in allergic keratoconjunctivitis. Ophthalmology 113 12623809
2003 Concerted expression of eotaxin-1, eotaxin-2, and eotaxin-3 in human bronchial epithelial cells. Cellular immunology 107 14698143
2000 Identification of potent, selective non-peptide CC chemokine receptor-3 antagonist that inhibits eotaxin-, eotaxin-2-, and monocyte chemotactic protein-4-induced eosinophil migration. The Journal of biological chemistry 97 10969084
2001 Rhinovirus infection up-regulates eotaxin and eotaxin-2 expression in bronchial epithelial cells. Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 94 11467997
2003 Eotaxin-2 and IL-5 cooperate in the lung to regulate IL-13 production and airway eosinophilia and hyperreactivity. The Journal of allergy and clinical immunology 90 14610483
2003 Significant elevation of serum levels of eotaxin-3/CCL26, but not of eotaxin-2/CCL24, in patients with atopic dermatitis: serum eotaxin-3/CCL26 levels reflect the disease activity of atopic dermatitis. Clinical and experimental immunology 89 14616792
2002 Eotaxin-2 generation is differentially regulated by lipopolysaccharide and IL-4 in monocytes and macrophages. Journal of immunology (Baltimore, Md. : 1950) 85 11823526
2012 Epithelial eotaxin-2 and eotaxin-3 expression: relation to asthma severity, luminal eosinophilia and age at onset. Thorax 83 23015684
2005 Eotaxin-2 and eotaxin-3 expression is associated with persistent eosinophilic bronchial inflammation in patients with asthma after allergen challenge. The Journal of allergy and clinical immunology 81 15805998
2006 Eosinophilic nasal polyps are a rich source of eotaxin, eotaxin-2 and eotaxin-3. Rhinology 71 16792175
1999 Glucocorticosteroids inhibit mRNA expression for eotaxin, eotaxin-2, and monocyte-chemotactic protein-4 in human airway inflammation with eosinophilia. Journal of immunology (Baltimore, Md. : 1950) 70 10415058
2019 Blockade of CCL24 with a monoclonal antibody ameliorates experimental dermal and pulmonary fibrosis. Annals of the rheumatic diseases 60 31129606
2006 Epithelial differentiation is a determinant in the production of eotaxin-2 and -3 by bronchial epithelial cells in response to IL-4 and IL-13. Molecular immunology 56 16740309
2007 Eotaxin-2 and colorectal cancer: a potential target for immune therapy. Clinical cancer research : an official journal of the American Association for Cancer Research 54 17908961
2000 NMR solution structure and receptor peptide binding of the CC chemokine eotaxin-2. Biochemistry 54 10913244
2010 Eotaxin-2/CCL24 and eotaxin-3/CCL26 exert differential profibrogenic effects on human lung fibroblasts. Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology 51 20143648
2001 Detection of mRNA for eotaxin-2 and eotaxin-3 in human dermal fibroblasts and their distinct activation profile on human eosinophils. The Journal of investigative dermatology 50 11286614
1998 Eotaxin-2 activates chemotaxis-related events and release of reactive oxygen species via pertussis toxin-sensitive G proteins in human eosinophils. European journal of immunology 50 9692884
2017 Anserine/Carnosine Supplementation Suppresses the Expression of the Inflammatory Chemokine CCL24 in Peripheral Blood Mononuclear Cells from Elderly People. Nutrients 49 29088099
2024 Mechanical stiffness promotes skin fibrosis via Piezo1-Wnt2/Wnt11-CCL24 positive feedback loop. Cell death & disease 48 38267432
2015 Eosinophils in Colorectal Neoplasms Associated with Expression of CCL11 and CCL24. Journal of pathology and translational medicine 47 26657310
2003 Th2- and to a lesser extent Th1-type cytokines upregulate the production of both CXC (IL-8 and gro-alpha) and CC (RANTES, eotaxin, eotaxin-2, MCP-3 and MCP-4) chemokines in human airway epithelial cells. International archives of allergy and immunology 46 12915769
2020 A blocking monoclonal antibody to CCL24 alleviates liver fibrosis and inflammation in experimental models of liver damage. JHEP reports : innovation in hepatology 45 32039405
2012 New biomarker for neovascular age-related macular degeneration: eotaxin-2. DNA and cell biology 43 23025269
2009 Interleukin-13 directly promotes oesophagus production of CCL11 and CCL24 and the migration of eosinophils. Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 43 20030665
2005 Cytokine-stimulated human lung alveolar epithelial cells release eotaxin-2 (CCL24) and eotaxin-3 (CCL26). Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 43 15695929
2010 Analysis of eotaxin 1/CCL11, eotaxin 2/CCL24 and eotaxin 3/CCL26 expression in lesional and non-lesional skin of patients with atopic dermatitis. Cytokine 39 20236835
2009 Genetic variability in CRTH2 polymorphism increases eotaxin-2 levels in patients with aspirin exacerbated respiratory disease. Allergy 36 19796209
2003 RANTES, eotaxin and eotaxin-2 expression and production in patients with aspirin triad. Allergy 36 14616128
2002 Regulatory effects of eotaxin, eotaxin-2, and eotaxin-3 on eosinophil degranulation and superoxide anion generation. Experimental biology and medicine (Maywood, N.J.) 36 12192108
2020 Blocking the autocrine regulatory loop of Gankyrin/STAT3/CCL24/CCR3 impairs the progression and pazopanib resistance of clear cell renal cell carcinoma. Cell death & disease 35 32051393
2023 CCL24 regulates biliary inflammation and fibrosis in primary sclerosing cholangitis. JCI insight 34 37345655
2011 Nasal lavage CCL24 levels correlate with eosinophils trafficking and symptoms in chronic sino-nasal eosinophilic inflammation. Rhinology 33 21743872
2022 CCL24/CCR3 axis plays a central role in angiotensin II-induced heart failure by stimulating M2 macrophage polarization and fibroblast activation. Cell biology and toxicology 30 36131165
2014 Nasal fluid release of eotaxin-3 and eotaxin-2 in persistent sinonasal eosinophilic inflammation. International forum of allergy & rhinology 30 24989688
2013 Control of extravillous trophoblast function by the eotaxins CCL11, CCL24 and CCL26. Human reproduction (Oxford, England) 30 23477905
2015 A CCL24-dependent pathway augments eosinophilic airway inflammation in house dust mite-challenged Cd163(-/-) mice. Mucosal immunology 28 26376364
2017 Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity. Scientific reports 25 28785009
2015 Chelidonine, a principal isoquinoline alkaloid of Chelidonium majus, attenuates eosinophilic airway inflammation by suppressing IL-4 and eotaxin-2 expression in asthmatic mice. Pharmacological reports : PR 24 26481537
2010 Protective effect of eotaxin-2 inhibition in adjuvant-induced arthritis. Clinical and experimental immunology 22 20456418
2004 The suggestive association of eotaxin-2 and eotaxin-3 gene polymorphisms in Korean population with allergic rhinitis. Immunogenetics 22 15580493
2016 Clinical Usefulness of Simultaneous Measurement of the Tear Levels of CCL17, CCL24, and IL-16 for the Biomarkers of Allergic Conjunctival Disorders. Current eye research 21 27897453
2008 Airway eosinophil accumulation and eotaxin-2/CCL24 expression following allergen challenge in BALB/c mice. Experimental lung research 19 18850374
2006 Endothelial and epithelial expression of eotaxin-2 (CCL24) in nasal polyps. International archives of allergy and immunology 19 16682802
2021 CCL24 Signaling in the Tumor Microenvironment. Advances in experimental medicine and biology 18 34286443
2020 Genetic control of CCL24, POR, and IL23R contributes to the pathogenesis of sarcoidosis. Communications biology 17 32826979
2006 Eotaxin-2 in sputum cell culture to evaluate asthma inflammation. The European respiratory journal 17 17079258
2023 Eosinophil trafficking in allergen-mediated pulmonary inflammation relies on IL-13-driven CCL-11 and CCL-24 production by tissue fibroblasts and myeloid cells. The journal of allergy and clinical immunology. Global 16 37781651
2014 Intraepithelial lymphocyte eotaxin-2 expression and perineural mast cell degranulation differentiate allergic/eosinophilic colitis from classic IBD. Journal of pediatric gastroenterology and nutrition 16 24813533
2018 Mesenchymal Stromal Cell (MSC)-Derived Combination of CXCL5 and Anti-CCL24 Is Synergistic and Superior to MSC and Cyclosporine for the Treatment of Graft-versus-Host Disease. Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation 15 29883796
2013 Trophoblasts-derived chemokine CCL24 promotes the proliferation, growth and apoptosis of decidual stromal cells in human early pregnancy. International journal of clinical and experimental pathology 15 23696919
2002 Eotaxin-2 alters eosinophil integrin function via mitogen-activated protein kinases. American journal of respiratory cell and molecular biology 15 12034562
2019 The proteolytic effect of mast cell tryptase to eotaxin-1/CCL11·eotaxin-2/CCL24 and eotaxin-3/CCL26 produced by conjunctival fibroblasts. Japanese journal of ophthalmology 14 30796548
2013 Alendronate attenuates eosinophilic airway inflammation associated with suppression of Th2 cytokines, Th17 cytokines, and eotaxin-2. Journal of immunology (Baltimore, Md. : 1950) 14 23935198
2005 Association of eotaxin-2 gene polymorphisms with plasma eotaxin-2 concentration. Journal of human genetics 14 15744457
2005 The association of eotaxin-2 and eotaxin-3 gene polymorphisms in a Korean population with ulcerative colitis. Experimental & molecular medicine 14 16391516
2003 Inhibition of CCL11, CCL24, and CCL26-induced degranulation in HL-60 eosinophilic cells by specific inhibitors of MEK1/MEK2, p38 MAP kinase, and PI 3-kinase. Immunopharmacology and immunotoxicology 14 12784909
2020 Increased CCL24 and CXCL7 levels in the cerebrospinal fluid of patients with neurosyphilis. Journal of clinical laboratory analysis 13 32419252
2024 The Role of CCL24 in Primary Sclerosing Cholangitis: Bridging Patient Serum Proteomics to Preclinical Data. Cells 11 38334601
2016 Tumor progression locus 2 reduces severe allergic airway inflammation by inhibiting Ccl24 production in dendritic cells. The Journal of allergy and clinical immunology 11 27484038
2015 Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy. Reproduction (Cambridge, England) 11 26316550
2020 Involvement of Eotaxins (CCL11, CCL24, CCL26) in Pathogenesis of Osteopenia and Osteoporosis. Iranian journal of public health 10 33643953
2016 Eotaxin-2 increased toll-like receptor 4 expression in endothelial cells in vitro and exacerbates high-cholesterol diet-induced atherogenesis in vivo. American journal of translational research 9 28078007
2012 Expression of RANTES, eotaxin-2, ICAM-1, LFA-1 and CCR-3 in chronic rhinosinusitis patients with nasal polyposis. Acta cirurgica brasileira 9 22936091
2015 Physiologic concentrations of HMGB1 have no impact on cytokine-mediated eosinophil survival or chemotaxis in response to Eotaxin-2 (CCL24). PloS one 8 25774667
2003 Backbone dynamics of the CC-chemokine eotaxin-2 and comparison among the eotaxin group chemokines. Proteins 8 12486712
2024 Machine Learning Identifies Key Proteins in Primary Sclerosing Cholangitis Progression and Links High CCL24 to Cirrhosis. International journal of molecular sciences 7 38892228
2007 Production and regulation of eotaxin-2/CCL24 in a differentiated human leukemic cell line, HT93. Biological & pharmaceutical bulletin 7 17917245
2025 Macrophage-Derived CCL24 Promotes Cardiac Fibrosis Via Fibroblast CCR3. Circulation research 6 40955564
2004 The chemokines CCL11, CCL20, CCL21, and CCL24 are preferentially expressed in polarized human secondary lymphoid follicles. The Journal of pathology 6 15376263
2023 CCL24, CXCL9 and CXCL10 are increased in synovial fluid in patients with juvenile idiopathic arthritis requiring advanced treatment. Rheumatology (Oxford, England) 5 36342195
2023 C-C Motif Chemokine Receptor 3-Mediated Extracellular Signal-Regulated Kinase 1/2 and p38 Mitogen-Activated Protein Kinase Signaling: Promising Targets for Human Airway Epithelial Mucin 5AC Induction by Eotaxin-2 and Eotaxin-3. International archives of allergy and immunology 5 37552963
2014 All eotaxins CCL11, CCL24 and CCL26 are increased but to various extents in pulmonary tuberculosis patients. Clinical laboratory 5 24600981
2021 CCL24 Protects Renal Function by Controlling Inflammation in Podocytes. Disease markers 4 34221188
2018 Eotaxin-2 induces monocytic apoptosis in patients who have undergone coronary artery bypass surgery and in THP-1 cells in vitro regulated by thrombomodulin. American journal of translational research 4 30416656
2017 TPL-2 restricts Ccl24-dependent immunity to Heligmosomoides polygyrus. PLoS pathogens 4 28759611
2025 CCL24 and Fibrosis: A Narrative Review of Existing Evidence and Mechanisms. Cells 3 39851534
2023 The Role of CCL24 in Systemic Sclerosis. Rambam Maimonides medical journal 3 37555717
2023 Downregulation of Salt-Inducible Kinase 3 Enhances CCL24 Activation in the Placental Environment with Preeclampsia. International journal of molecular sciences 3 38203391
2011 Increased CCL24/eotaxin-2 with postnatal ozone exposure in allergen-sensitized infant monkeys is not associated with recruitment of eosinophils to airway mucosa. Toxicology and applied pharmacology 3 21945493
2022 Eotaxin-2 and eotaxin-3 in malaria exposure and pregnancy. Malaria journal 2 36380370
2025 Distinct Roles Between Eotaxin 1 and Eotaxin 2 in Asthmatic Airways. Clinical and translational allergy 1 40650924
2021 Nodal histiocytic sarcoma with prominent eosinophilic infiltration: expression of eotaxin-2 on tumor cells. Diagnostic pathology 1 33436014
2009 [Effects of corticosteroid on Eotaxin and Eotaxin-2 in nasal polyps]. Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery 1 19522186
2001 Analysis of eosinophils and myeloid progenitor responses to modified forms of MPIF-2. Cytokine 1 11237428
2026 CCL24 recruits CCR3+ TAMs to promote immunosuppression via YAP1 activation and serves as a therapeutic target for Gracillin in colorectal cancer. International journal of biological sciences 0 41694595
2026 Peritoneal MSCs-derived exosomes suppress CCL24 synthesis through miR-320d delivery contributing to the improvement of peritoneal dialysis-associated fibrosis. Scientific reports 0 41781517
2026 EBF3 suppresses lung adenocarcinoma progression and immune evasion via transcriptional repression of CCL24. Cellular oncology (Dordrecht, Netherlands) 0 42018103
2025 mTORC1-Dependent Regulation of the CCL24-CCR3 Axis Controls Granuloma Formation and Maintenance in Sarcoidosis. bioRxiv : the preprint server for biology 0 40791394
2007 [Expression and significance of Eotaxin and Eotaxin-2 in nasal polyposis and nasal polyp tissue]. Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery 0 17438849