Affinage

CCL24

C-C motif chemokine 24 · UniProt O00175

Length
119 aa
Mass
13.1 kDa
Annotated
2026-06-09
98 papers in source corpus 33 papers cited in narrative 33 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CCL24 (eotaxin-2) is a secreted CC chemokine that signals exclusively through the G protein-coupled receptor CCR3, which it engages by binding a CCR3 N-terminal peptide into a groove at the interface of its N-loop and β2–β3 hairpin, a fold defined by NMR as a three-stranded antiparallel β-sheet packed against a C-terminal α-helix and tethered by conserved disulfide bonds (PMID:9182688, PMID:10913244). Its N-terminus is the activity determinant: progressive truncation abolishes agonist function and an N-terminally truncated form converts CCL24 into a CCR3 antagonist while retaining myeloid progenitor inhibitory activity, establishing separable structural determinants (PMID:11237428). In its canonical role CCL24 drives eosinophil and basophil recruitment and effector functions — chemotaxis, calcium flux, actin polymerization, ROS release, and degranulation — through CCR3 coupled to pertussis toxin-sensitive Gi proteins and downstream ERK1/2, p38 MAPK, and PI3K cascades, and it switches eosinophil integrin usage from VLA-4/VCAM-1 to LFA-1/ICAM-1 (PMID:9182688, PMID:9692884, PMID:12034562, PMID:12784909). In vivo, CCL24 acts within the IL-13/STAT6 axis to mediate allergen- and IL-13-driven airway eosinophilia, cooperating with IL-5 to produce airway hyperreactivity; CCL24 production is itself induced by IL-13 through STAT6 in macrophages, oesophageal tissue, and epithelia and is restrained by TPL-2 kinase in dendritic cells and by CD163 in macrophages (PMID:11067944, PMID:15647285, PMID:14610483, PMID:27484038, PMID:26376364, PMID:20030665). Beyond inflammation, macrophage-derived CCL24 is a central driver of organ fibrosis: it activates fibroblasts, hepatic stellate cells, cholangiocytes, and cardiac fibroblasts via CCR3/PI3K and TGF-β, and genetic deletion of CCL24 or fibroblast-specific CCR3, or antibody blockade with CM-101, attenuates dermal, pulmonary, hepatic, biliary, and cardiac fibrosis (PMID:20143648, PMID:31129606, PMID:32039405, PMID:40955564, PMID:37345655). CCL24 also promotes trophoblast invasion via ERK1/2–PI3K–MMP9, induces airway epithelial MUC5AC through CCR3–ERK1/2–p38, and sustains a tumor-promoting autocrine gankyrin/STAT3/CCL24/CCR3 loop in renal cell carcinoma (PMID:26316550, PMID:32051393, PMID:37552963).

Mechanistic history

Synthesis pass · year-by-year structured walk · 30 steps
  1. 1997 High

    Established that CCL24's biological activity is mediated exclusively through CCR3, defining its receptor specificity and target-cell selectivity for eosinophils and basophils.

    Evidence Chemotaxis, Ca2+ mobilization, histamine/LTC4 release with CCR3-blocking mAb and cross-desensitization, plus intradermal injection in primate

    PMID:9182688

    Open questions at the time
    • Did not resolve downstream signaling components
    • Did not address non-immune cell responses later found in fibrosis and cancer
  2. 1998 High

    Defined the receptor-coupling logic by showing CCR3 signals through pertussis toxin-sensitive Gi proteins to drive eosinophil actin polymerization and ROS release.

    Evidence NBD-phallacidin flow cytometry, ROS chemiluminescence, pertussis toxin and CCR3-blocking mAb

    PMID:9692884

    Open questions at the time
    • Specific G protein isoform not identified
    • Did not map kinase cascades downstream of Gi
  3. 2000 High

    Determined the three-dimensional fold of CCL24 and localized the CCR3 N-terminal binding site to the N-loop/β2–β3 groove, providing a structural basis for receptor engagement.

    Evidence Heteronuclear NMR structure determination with receptor peptide binding shift/line-broadening assay

    PMID:10913244

    Open questions at the time
    • No full-length receptor complex structure
    • Binding affinity and stoichiometry not quantified
  4. 2000 High

    Identified the upstream IL-4/STAT6 induction of CCL24 in the lung and confirmed its eosinophil-selective chemotactic action.

    Evidence Northern blot in allergen-challenged and IL-4 transgenic mice, STAT6 KO epistasis, recombinant protein chemotaxis

    PMID:11067944

    Open questions at the time
    • Did not separate IL-4 from IL-13 contributions
    • Cell-type source of CCL24 not defined
  5. 2001 High

    Mapped the N-terminus as the agonist determinant and produced a CCR3 antagonist, separating eosinophil-activating from myeloid-inhibitory functions.

    Evidence Amino-terminal deletion mutagenesis with calcium, chemotaxis, binding, and colony-formation readouts

    PMID:11237428

    Open questions at the time
    • Structural basis of the antagonist conformation not solved
    • Myeloid inhibitory receptor not identified
  6. 2002 High

    Resolved the cell-source regulation of CCL24, showing constitutive monocyte production with differentiation- and cytokine-dependent switching to IL-4-driven macrophage production.

    Evidence Primary monocyte/macrophage culture with cytokine stimulation and CCL24 ELISA across differentiation states

    PMID:11823526

    Open questions at the time
    • Transcriptional mechanism of differentiation switch not defined
    • Did not address fibroblast production seen in later disease contexts
  7. 2002 High

    Demonstrated that CCL24 reprograms eosinophil adhesion by shifting integrin usage from VLA-4/VCAM-1 to LFA-1/ICAM-1 via CCR3 and MEK/ERK signaling.

    Evidence Parallel-plate flow chamber adhesion assay with adhesion-molecule and CCR3 mAbs and MEK inhibitor

    PMID:12034562

    Open questions at the time
    • In vivo relevance of the integrin switch not tested
    • Did not address p38 or PI3K roles in adhesion
  8. 2003 Medium

    Defined the kinase cascade (ERK1/2, p38, PI3K) required for CCL24-induced eosinophil degranulation, connecting receptor coupling to effector output.

    Evidence EPO degranulation assay with U0126, SB203580, LY294002 and IL-5 co-stimulation in eosinophilic cell model

    PMID:12784909

    Open questions at the time
    • Cell-line model rather than primary eosinophils
    • Did not establish branch-point hierarchy among the kinases
  9. 2003 High

    Showed in vivo that CCL24 cooperates with IL-5 to drive eosinophilia and airway hyperreactivity, with the effector axis dependent on CCR3 and the IL-4Rα/IL-13/STAT6 pathway.

    Evidence Recombinant CCL24 instillation in IL-5 transgenic mice, anti-CCR3 mAb, IL-4Rα/IL-13/STAT6 KO mice, methacholine AHR

    PMID:14610483

    Open questions at the time
    • Did not isolate the direct CCL24 target cell for AHR
    • Endogenous CCL24 requirement not tested by genetic deletion here
  10. 2005 High

    Used genetic deletion to place CCL24 downstream of IL-13 and establish it as a non-redundant driver of luminal (airway) eosinophilia distinct from tissue-restricted CCL11.

    Evidence IL-13 KO, CCL24 KO, and IL-13 lung transgenic compound mice with airway compartment analysis

    PMID:15647285

    Open questions at the time
    • Molecular basis of compartmental specialization vs CCL11 not defined
    • Baseline tissue eosinophil homeostasis unaffected, leaving its physiologic role open
  11. 2007 Medium

    Identified GATA-1 as a transcriptional controller of CCL24 production during eosinophilic lineage differentiation.

    Evidence ATRA differentiation of HT93 cells with GATA-1 siRNA knockdown and overexpression, CCL24 ELISA

    PMID:17917245

    Open questions at the time
    • Direct GATA-1 binding to CCL24 promoter not shown
    • Cell-line model only
  12. 2010 Medium

    Extended CCL24 function beyond leukocyte chemotaxis by showing it directly stimulates lung fibroblast proliferation and collagen synthesis, an eotaxin-specific activity not shared by CCL26.

    Evidence Thymidine incorporation, hydroxyproline assays, Boyden chamber, α-SMA staining on primary human lung fibroblasts

    PMID:20143648

    Open questions at the time
    • Receptor and signaling pathway in fibroblasts not dissected here
    • No α-SMA induction, leaving myofibroblast conversion mechanism unresolved
  13. 2009 High

    Confirmed IL-13Rα1/STAT6 as the inductive pathway for CCL24 at the tissue level and demonstrated functional sufficiency for eosinophil recruitment.

    Evidence Isolated oesophageal ring cultures from WT and STAT6 KO mice with IL-13 stimulation and eosinophil migration assay

    PMID:20030665

    Open questions at the time
    • Tissue cell source of CCL24 within the oesophagus not pinpointed
    • Temporal CCL11-then-CCL24 ordering mechanism unexplained
  14. 2013 Medium

    Revealed a reproductive role in which CCL24 promotes trophoblast invasion and adhesion via MMP2 activation, broadening its activity to non-immune tissue remodeling.

    Evidence Real-time migration, Matrigel invasion, zymography, and ECM adhesion assays in HTR8/SVneo cells

    PMID:23477905

    Open questions at the time
    • Receptor dependence not validated with CCR3 blockade
    • Cell-line and in vitro only
  15. 2015 Medium

    Defined the trophoblast invasion mechanism as CCR3-driven ERK1/2 and PI3K signaling activating Ki67 and MMP9, and identified hormonal control of the CCL24/CCR3 system.

    Evidence Pathway inhibitor panel, downstream Ki67/MMP9 readouts, co-culture and hormone treatment

    PMID:26316550

    Open questions at the time
    • In vivo relevance to implantation not established
    • Single cell-line model
  16. 2016 High

    Established negative regulation of CCL24 by TPL-2 kinase in dendritic cells as a brake on airway eosinophilia, defining a cell-type-specific upstream control point.

    Evidence Map3k8-/- mice, conditional KO, adoptive DC transfer, anti-CCL24 neutralizing antibody

    PMID:27484038

    Open questions at the time
    • Mechanism linking TPL-2 signaling to CCL24 transcription not defined
    • Restricted to dendritic cells
  17. 2015 High

    Identified CD163-mediated allergen scavenging as an upstream suppressor of macrophage CCL24, controlling airway eosinophilia and mucous metaplasia.

    Evidence Cd163-/- mice, proteomic CD163–Der p1 pulldown, anti-CCL24 antibody rescue, adoptive macrophage transfer

    PMID:26376364

    Open questions at the time
    • Intracellular link between CD163 signaling and CCL24 transcription unresolved
    • Specific to HDM allergen context
  18. 2016 Medium

    Showed CCL24 acts on endothelium to upregulate TLR4 and promote monocyte adhesion, implicating it in atherosclerosis via MAPK signaling and RNA/protein stabilization machinery.

    Evidence TLR4 siRNA, MAPK inhibitors, HuR/TTP/PRAT4A analysis, monocyte adhesion, Ldlr/Tlr4 double-KO mice

    PMID:28078007

    Open questions at the time
    • Receptor mediating CCL24's endothelial effect not confirmed as CCR3
    • Single lab
  19. 2017 Medium

    Linked commensal microbiota to CCL24 control, showing antibiotic depletion raises macrophage CCL24, drives M2 polarization, and impairs γδT cell anti-tumor responses.

    Evidence Antibiotic-treated mice, alveolar macrophage profiling, adoptive transfer, anti-CCL24 antibody, B16/F10 tumor model

    PMID:28785009

    Open questions at the time
    • Microbial signal regulating CCL24 not identified
    • CCR3 dependence of γδT effect not tested
  20. 2019 High

    Demonstrated that antibody blockade of CCL24 (CM-101) inhibits fibroblast-to-myofibroblast transition and reduces fibrosis in vivo, validating CCL24 as a therapeutic target in fibrotic disease.

    Evidence Skin fibroblast and endothelial activation assays with SSc serum ± CM-101, bleomycin dermal and pulmonary fibrosis models

    PMID:31129606

    Open questions at the time
    • Receptor and intracellular pathway in fibroblasts not fully dissected here
    • Cellular source of CCL24 in disease not pinpointed
  21. 2020 High

    Established CCL24/CCR3 as a driver of liver fibrosis through hepatic stellate cell activation using both genetic deletion and antibody blockade across multiple models.

    Evidence Ccl24 KO mice, CM-101 in MCD/STAM/TAA models, LX2 motility/α-SMA/pro-collagen assays

    PMID:32039405

    Open questions at the time
    • Cellular source of hepatic CCL24 not defined in this study
    • Signaling pathway in HSCs not dissected here
  22. 2020 High

    Defined an autocrine gankyrin/STAT3/CCL24/CCR3 loop driving renal cell carcinoma drug resistance and metastasis, connecting CCL24 transcription to a tumor-promoting feedback circuit.

    Evidence Co-IP, ChIP at CCL24 promoter, CCR3 inhibitor SB328437, gankyrin knockdown, in vivo metastasis models

    PMID:32051393

    Open questions at the time
    • Generality across other tumor types not established
    • Downstream effectors of CCR3 in this loop not mapped
  23. 2022 Medium

    Showed the CCL24/CCR3 axis drives M2 macrophage polarization and cardiac fibroblast activation, extending the fibrotic role to the heart.

    Evidence RNA-seq, CyTOF, immunofluorescence co-localization, fibroblast activation assays, Ang II mouse model with anti-CCL24 antibody

    PMID:36131165

    Open questions at the time
    • Direct vs indirect fibroblast effect not separated here
    • Single lab
  24. 2023 High

    Extended CCL24 fibrogenic action to the biliary compartment, showing it induces hepatic stellate cell and cholangiocyte proliferation with CM-101 improving cholestatic fibrosis.

    Evidence Mdr2-/- PSC model with CM-101, spatial transcriptomics, primary human HSC and cholangiocyte assays

    PMID:37345655

    Open questions at the time
    • Receptor identity on cholangiocytes not confirmed
    • Signaling pathway not dissected here
  25. 2023 Medium

    Defined CCR3-ERK1/2-p38 as the pathway by which CCL24 induces airway epithelial MUC5AC, linking CCL24 to mucus production.

    Evidence Inhibitor and siRNA dissection of ERK1/2/p38 with MUC5AC readouts in NCI-H292 and primary nasal epithelial cells

    PMID:37552963

    Open questions at the time
    • In vivo contribution to airway mucus not established
    • Single lab
  26. 2025 High

    Provided definitive genetic proof that cardiac resident macrophage CCL24 directly activates cardiac fibroblasts via CCR3 and PI3K/TGF-β in an inflammation-independent manner.

    Evidence CCL24 KO and fibroblast-specific CCR3 CRISPR/Cas9 KO mice in TAC model, primary fibroblast assays with PI3K inhibitors, in vivo blockade

    PMID:40955564

    Open questions at the time
    • Mechanism of PI3K-to-TGF-β coupling in fibroblasts not fully detailed
    • Translation to human cardiac fibrosis not shown
  27. 2024 Medium

    Revealed a mechanosensitive feedback loop in which matrix stiffness drives Piezo1/Wnt-dependent CCL24 secretion that further stiffens the dermal microenvironment.

    Evidence Piezo1 knockdown on stiffness-tuned substrates, Wnt2/Wnt11 analysis, CCL24 ELISA, in vivo bleomycin model

    PMID:38267432

    Open questions at the time
    • Direct transcriptional link between Wnt signaling and CCL24 not established
    • Single lab
  28. 2025 Medium

    Identified mTORC1/STAT3 as a fibroblast pathway suppressing CCL24 and controlling granuloma formation, adding a metabolic regulatory layer.

    Evidence Conditional Tsc1/Tsc2 Fsp1-Cre KO mice, chemokine array, STAT3 analysis, rapamycin/azithromycin rescue

    PMID:42246493

    Open questions at the time
    • Direct STAT3 occupancy at the CCL24 locus not shown
    • Single study
  29. 2026 Medium

    Established CCL24 as a direct mediator of EBF3-controlled immune remodeling in lung adenocarcinoma, driving M2 polarization and suppressing T-cell recruitment.

    Evidence EBF3 overexpression/knockdown, syngeneic tumor model, immune infiltrate flow cytometry, in vivo CCL24 rescue

    PMID:42018103

    Open questions at the time
    • Receptor mediating tumor immune effects not confirmed
    • Single lab, emerging study
  30. 2026 Medium

    Defined macrophage-derived CCL24 driving mesothelial-to-mesenchymal transition via CCR3/p38 in peritoneal fibrosis and identified miR-320d/KLF7/STAT3 as upstream suppressors.

    Evidence CCL24 macrophage knockdown, CCR3/p38 inhibition, miR-320d exosome delivery, KLF7 target validation, rat PD model

    PMID:41781517

    Open questions at the time
    • Direct KLF7-STAT3-CCL24 transcriptional link relies on single-model data
    • Human relevance not shown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CCL24 selects between its eosinophil-activating, fibroblast-activating, and tumor-immune-modulating outputs through a single CCR3 receptor, and whether the non-CCR3 endothelial activity represents a distinct receptor, remains unresolved.
  • No structural model of full-length CCL24–CCR3 complex
  • Mechanism distinguishing chemotactic vs fibrogenic signaling bias unknown
  • Receptor mediating endothelial/atherosclerotic effects not confirmed as CCR3

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 4 GO:0060089 molecular transducer activity 3
Localization
GO:0005576 extracellular region 3
Pathway
R-HSA-1474244 Extracellular matrix organization 4 R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 4
Partners
CCR3

Evidence

Reading pass · 33 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 CCL24 (eotaxin-2) acts exclusively via CCR3: chemotaxis of eosinophils and basophils, histamine and leukotriene C4 release from IL-3-primed basophils, and Ca2+ mobilization in eosinophils were all abrogated by a CCR3-blocking monoclonal antibody; complete cross-desensitization was observed between CCL24, eotaxin, and MCP-4, confirming shared CCR3 usage. No responses were observed in neutrophils, monocytes, or lymphocytes. Chemotaxis assay, Ca2+ mobilization, histamine/LTC4 release, CCR3-blocking mAb, receptor cross-desensitization, intradermal injection in rhesus monkey The Journal of experimental medicine High 9182688
2000 NMR solution structure of CCL24 (73 aa) determined: a helical turn (residues 17–20), 3-stranded antiparallel β-sheet (residues 22–26, 37–41, 44–49), and an α-helix (residues 54–66), with two conserved disulfide bonds tethering the N-terminal/N-loop to the β-sheet. An N-terminal peptide of CCR3 binds into a groove at the interface of the N-loop and β2–β3 hairpin of CCL24, with additional contacts at the N-terminus and part of the α-helix. Heteronuclear and triple-resonance NMR, distance geometry–simulated annealing structure calculation, receptor peptide binding NMR shift/line-broadening assay Biochemistry High 10913244
2000 CCL24 requires an intact N-terminus for eosinophil activity: deletion of the first two amino acids did not markedly alter calcium mobilization, chemotaxis, or receptor binding, whereas further truncations caused complete loss of eosinophil agonist activity. An N-terminally truncated mutant (P30–R99) converted CCL24 from agonist to antagonist of CCR3-mediated eosinophil calcium flux and chemotaxis, yet retained myeloid progenitor inhibitory activity, demonstrating separable structural determinants for the two activities. Amino-terminal deletion mutagenesis, calcium mobilization assay, chemotaxis assay, receptor binding, myeloid progenitor colony formation assay Cytokine High 11237428
1998 CCL24 activates eosinophil actin polymerization, reactive oxygen species (ROS) release, and chemotaxis via CCR3 coupled to pertussis toxin-sensitive Gi proteins; CCR3-blocking mAb 7B11 inhibited CCL24-induced Ca2+ mobilization and ROS release, and pertussis toxin blocked ROS release, demonstrating Gi coupling downstream of CCR3. NBD-phallacidin/flow cytometry (actin polymerization), ROS chemiluminescence assay, pertussis toxin treatment, CCR3-blocking mAb, Ca2+ mobilization European journal of immunology High 9692884
2002 CCL24 alters eosinophil integrin usage via CCR3 and MAP kinases: immobilized CCL24 reduced eosinophil adhesion to VCAM-1 and increased adhesion to ICAM-1 under physiologic shear stress, shifting integrin usage from VLA-4/VCAM-1 to LFA-1/ICAM-1-dominated pathways. Both a CCR3-blocking mAb and the MEK inhibitor PD98059 prevented these changes. Parallel-plate flow chamber adhesion assay, adhesion molecule-blocking mAbs, CCR3-blocking mAb, MEK inhibitor (PD98059), video microscopy American journal of respiratory cell and molecular biology High 12034562
2003 CCR3-mediated CCL24-induced eosinophil degranulation (eosinophil peroxidase release) requires activation of ERK1/ERK2, p38 MAP kinase, and PI3-kinase; specific inhibitors U0126, SB203580, and LY294002 each concentration-dependently reduced CCL24-induced EPO degranulation. IL-5 potentiated CCL24-induced degranulation. EPO degranulation assay with specific kinase inhibitors (U0126, SB203580, LY294002), IL-5 co-stimulation, HL-60 eosinophilic cell model Immunopharmacology and immunotoxicology Medium 12784909
2002 Peripheral blood monocytes constitutively produce bioactive CCL24 protein; production is up-regulated by IL-1β, LPS, and zymosan but not by IL-4, IL-13, or TNF-α alone. IL-4 suppresses LPS-stimulated CCL24 from monocytes. Upon differentiation to macrophages, constitutive CCL24 production is suppressed, but IL-4 (not LPS) then up-regulates macrophage CCL24 production. Human dermal fibroblasts do not produce CCL24 under basal or stimulated conditions. Primary monocyte/macrophage culture, cytokine stimulation, ELISA for CCL24 protein, monocyte-to-macrophage differentiation Journal of immunology High 11823526
2000 Murine eotaxin-2 mRNA is induced in the lung by allergen challenge (Aspergillus fumigatus, OVA) and by transgenic or intranasal IL-4; IL-4-induced expression requires STAT6, as demonstrated by genetic ablation of STAT6 in IL-4 transgenic mice. Recombinant murine CCL24 protein induces dose-dependent eosinophil chemotaxis (1–1000 ng/ml) but has no activity on macrophages or neutrophils. Northern blot, transgenic/knockout mice (IL-4 tg, STAT6-deficient), intranasal IL-4, recombinant protein chemotaxis assay Journal of immunology High 11067944
2005 IL-13 is required for allergen-induced CCL24 (and CCL11) expression in the lung: ovalbumin-induced eotaxin-1 and eotaxin-2 mRNA were almost completely abolished in IL-13 gene-targeted mice. CCL24 deficiency (CCL24 KO mice) does not affect baseline eosinophil levels in hematopoietic tissues or the GI tract, but profoundly reduces airway eosinophilia following intratracheal IL-13 administration. CCL24 is expressed by macrophages in luminal (airway) compartments, while CCL11 is expressed solely in tissue. In IL-13 lung transgenic/CCL24 KO compound mice, luminal eosinophils are markedly reduced. IL-13 KO mice, CCL24 KO mice (homologous recombination), IL-13 lung transgenic mice, intratracheal IL-13 administration, lung compartment analysis The Journal of biological chemistry High 15647285
2003 CCL24 and IL-5 cooperate to promote pulmonary eosinophil accumulation, IL-13 production, and airway hyperreactivity (AHR) to methacholine; neither agent alone induced these features. AHR was dependent on IL-13 and signaling through IL-4Rα/STAT6, and the eosinophil accumulation required CCR3, as demonstrated by anti-CCR3 mAb blockade. CCL24-induced features were absent in IL-4Rα-deficient, IL-13-deficient, or STAT6-deficient mice. Recombinant CCL24 instillation in IL-5-treated or IL-5 transgenic mice, methacholine AHR measurement, anti-CCR3 mAb blockade, IL-4Rα/IL-13/STAT6 KO mice The Journal of allergy and clinical immunology High 14610483
2003 NMR backbone dynamics of CCL24 show highly restricted motion in the first two β-strands and α-helix on sub-nanosecond timescales, with substantial flexibility in N- and C-terminal regions and the N-loop/third β-strand groove (the likely CCR3 N-terminal binding site), consistent with conformational rearrangements occurring during receptor binding. 15N NMR relaxation measurements, backbone dynamics analysis Proteins Medium 12486712
2010 CCL24 (but not CCL26/eotaxin-3) stimulates human lung fibroblast proliferation and collagen synthesis; CCL26 (but not CCL24) promotes fibroblast migration. Neither CCL24 nor CCL26 induces α-smooth muscle actin expression or TGF-β1 release from lung fibroblasts. [3H]-thymidine incorporation (proliferation), [3H]-hydroxyproline and biochemical staining (collagen), Boyden chamber chemotaxis, immunostaining for α-SMA, ELISA for TGF-β1 Annals of allergy, asthma & immunology Medium 20143648
2013 CCL24 promotes extravillous trophoblast (EVT) migration, invasion, and adhesion to collagen IV and fibronectin; all three eotaxins (CCL11, CCL24, CCL26) significantly increased HTR8/SVneo MMP2 activity without altering TIMP2 activity, providing a mechanism for enhanced invasion. xCELLigence real-time migration assay, wound-healing assay, Matrigel invasion assay, zymography (MMP2), reverse zymography (TIMP2), adhesion assay to ECM proteins Human reproduction Medium 23477905
2015 CCL24 promotes trophoblast proliferation, viability, and invasiveness via CCR3 acting through ERK1/2 and PI3K signaling pathways (not JNK or p38), activating downstream Ki67 and MMP9. Steroid hormones (progesterone, hCG) and co-culture with decidual stromal cells up-regulate CCL24 and CCR3 expression on trophoblasts. Functional proliferation/invasion/viability assays, pathway inhibitors (ERK1/2, PI3K, JNK, p38), Ki67 and MMP9 readouts, co-culture system, hormone treatment Reproduction (Cambridge, England) Medium 26316550
2019 Blockade of CCL24 with monoclonal antibody CM-101 inhibits CCL24-induced dermal fibroblast activation and transition to myofibroblasts, and inhibits endothelial cell activation. In bleomycin-induced mouse models, CM-101 profoundly inhibits both dermal and pulmonary fibrosis and inflammation. Skin fibroblast and endothelial cell activation assays with CCL24 or SSc serum ± CM-101, bleomycin prevention and treatment models in vivo (dermal and pulmonary fibrosis endpoints) Annals of the rheumatic diseases High 31129606
2020 CCL24 promotes liver fibrosis and inflammation via CCR3: Ccl24 knockout mice on MCD diet show reduced histological NAFLD activity scores, fibrosis, and liver enzymes compared to wild-type mice. CM-101 anti-CCL24 antibody inhibited CCL24-induced hepatic stellate cell (HSC) motility, α-SMA expression, and pro-collagen I secretion in the LX2 cell line, and reduced liver damage in three experimental models (MCD, STAM, TAA). Ccl24 KO mice (MCD diet model), CM-101 anti-CCL24 mAb in MCD/STAM/TAA models, LX2 HSC activation assays (motility, α-SMA, pro-collagen I), histology, liver enzymes JHEP reports High 32039405
2022 The CCL24/CCR3 axis promotes M2 macrophage polarization and cardiac fibroblast activation. In vitro, CCL24 acts through its G protein-coupled receptor CCR3 (confirmed by co-localization on macrophages and fibroblasts) to activate cardiac primary fibroblasts. In angiotensin II-induced heart failure mice, anti-CCL24 antibody decreased M2 macrophage and monocyte polarization and reduced cardiac hypertrophy and fibrosis. RNA-seq, CyTOF single-cell analysis, immunofluorescence co-localization (CCR3 on macrophages/fibroblasts), in vitro fibroblast activation assays, Ang II mouse model with anti-CCL24 antibody Cell biology and toxicology Medium 36131165
2025 Cardiac resident macrophages (CRMs) are the primary source of CCL24 in the heart during pressure overload. CCL24 deficiency (global KO) reduces cardiac fibrosis following transverse aortic constriction. CCL24 directly activates cardiac fibroblasts through CCR3 in an inflammation-independent process, promoting fibroblast proliferation and activation via PI3K signaling and TGF-β release. Fibroblast-specific CCR3 deletion (CRISPR/Cas9) phenocopies CCL24 KO in reducing fibrosis and improving cardiac function. CCL24 KO mice (transverse aortic constriction), fibroblast-specific CCR3 CRISPR/Cas9 KO mice, primary cardiac fibroblast activation assays with PI3K inhibitors, CCL24-blocking antibody and CCR3 antagonist in vivo Circulation research High 40955564
2024 Increased matrix stiffness drives CCL24 secretion by dermal fibroblasts through the mechanosensitive ion channel Piezo1 acting via the Wnt2/Wnt11 pathway; secreted CCL24 in turn stiffens the microenvironment to increase Piezo1 expression, forming a positive feedback loop. AAV-mediated Piezo1 knockdown ameliorated skin fibrosis progression and skin stiffness in mice. Piezo1 knockdown (AAV and siRNA) in dermal fibroblasts on stiffness-tuned substrates, Wnt2/Wnt11 pathway analysis, CCL24 ELISA, in vivo bleomycin/mechanical fibrosis model Cell death & disease Medium 38267432
2016 TPL-2 kinase in lung dendritic cells (DCs) negatively regulates CCL24 expression; TPL-2-deficient (Map3k8-/-) DCs express elevated CCL24, and blockade of CCL24 with a neutralizing antibody prevents the exaggerated airway eosinophilia and lung inflammation in mice given HDM-pulsed Map3k8-/- DCs. This was specific to DCs and not to T cells, B cells, or LysM+ myeloid cells. Map3k8-/- mice, bone marrow chimeras, conditional KO mice, adoptive DC transfer, anti-CCL24 neutralizing antibody, BAL differential cell counts, ELISA, RNA-seq The Journal of allergy and clinical immunology High 27484038
2015 CD163, a macrophage scavenger receptor, binds Der p1 (house dust mite allergen) in a calcium-dependent manner. Loss of CD163 leads to increased CCL24 production by bone marrow-derived macrophages upon Der p1 stimulation, and increased CCL24 mediates the augmented airway eosinophilia and mucous cell metaplasia in Cd163-/- HDM-challenged mice; neutralizing anti-CCL24 antibody reverses this phenotype. Cd163-/- mice (HDM and Der p1 challenge), proteomic pulldown (CD163–Der p1 binding), anti-CCL24 neutralizing antibody, BMMΦ CCL24 secretion assay, adoptive macrophage transfer Mucosal immunology High 26376364
2017 Commensal microbiota maintains alveolar macrophages with low CCL24 production; antibiotic-mediated depletion of commensals increases CCL24 from alveolar macrophages and promotes M2 polarization, which inhibits γδT cell-mediated anti-tumor responses. Adoptive transfer of normal alveolar macrophages or CCL24 antibody neutralization rescued the γδT17 cell frequency and anti-tumor response in antibiotic-treated mice. Antibiotic-treated mouse model, gene expression/protein analysis of alveolar macrophages, adoptive macrophage transfer, anti-CCL24 neutralizing antibody, B16/F10 tumor model, flow cytometry Scientific reports Medium 28785009
2020 In clear cell renal cell carcinoma, gankyrin recruits STAT3 via direct binding; STAT3 binds the CCL24 promoter and promotes CCL24 expression. Autocrine CCL24 signals back through CCR3 to further enhance gankyrin expression and STAT3 activation, forming a positive autocrine regulatory loop. Blocking this loop via gankyrin knockdown or the CCR3 inhibitor SB328437 reversed pazopanib resistance and inhibited lung metastasis in vivo. Co-IP (gankyrin–STAT3), ChIP (STAT3 at CCL24 promoter), CCR3 inhibitor (SB328437), gankyrin knockdown, in vivo subcutaneous and lung metastasis models, in vitro functional assays Cell death & disease High 32051393
2023 CCL24 induces proliferation of primary human hepatic stellate cells and cholangiocytes; in the Mdr2-/- mouse PSC model, CM-101 (CCL24-neutralizing antibody) improved biliary inflammation, fibrosis, and cholestasis markers and reduced cholangiocyte proliferation and senescence as shown by spatial transcriptomics. CCL24 is expressed by liver macrophages in this model. Mdr2-/- mice + CM-101 antibody treatment, spatial transcriptomics, primary human HSC and cholangiocyte proliferation assays, macrophage co-culture, ELISA, histology JCI insight High 37345655
2023 CCR3-mediated ERK1/2 and p38 MAPK signaling are required for CCL24-induced MUC5AC (mucin 5AC) expression in airway epithelial cells; CCR3 inhibition (SB328437), ERK1/2 inhibitor (U0126), p38 inhibitor (SB203580), and ERK1/2/p38 siRNA each suppressed CCL24-induced MUC5AC mRNA and protein in NCI-H292 cells and primary nasal epithelial cells. RT-PCR, ELISA, western blot (phospho-ERK1/2, phospho-p38), CCR3 inhibitor, MEK/p38 inhibitors, siRNA knockdown of ERK1/2 and p38, primary HNEpC cells International archives of allergy and immunology Medium 37552963
2025 mTORC1 suppresses CCL24 expression via aberrant STAT3 signaling in fibroblasts and promotes CCR3 expression in interstitial macrophages. In TSC1/TSC2-deleted (Fsp1-Cre) mice, loss of mTORC1 restraint leads to reduced CCL24 and sarcoid-like granuloma formation; rapamycin and azithromycin attenuated granuloma burden and normalized CCL24–CCR3 signaling. Conditional Tsc1/Tsc2 Fsp1-Cre KO mice, cytokine/chemokine array, STAT3 pathway analysis, rapamycin/azithromycin pharmacological treatment, granuloma histology Molecular and cellular biology Medium 42246493
2013 Trophoblasts secrete CCL24, while decidual stromal cells (DSCs) express CCR3. CCL24 promotes DSC proliferation and increases total DSC numbers while also increasing apoptosis; the net effect is increased cell numbers. DSC–trophoblast co-culture raises CCL24 levels and CCR3 expression on DSCs; estrogen, progesterone, and hCG up-regulate CCR3 on DSCs. Co-culture experiments, CCL24 ELISA, CCR3 expression assays, DSC proliferation/apoptosis readouts, hormone treatment International journal of clinical and experimental pathology Medium 23696919
2016 CCL24 increases TLR4 expression in human coronary artery endothelial cells (HCAECs) via JNK/SAPK, p38 MAPK, and ERK1/2 signaling, with post-transcriptional mRNA stabilization mediated by HuR/TTP RNA-binding proteins and protein trafficking regulated by the chaperone PRAT4A. TLR4 siRNA knockdown reversed CCL24-augmented monocyte adhesion to LPS-stimulated HCAECs. In LdlrTlr4 double-knockout mice (but not B6.129S7-Ldlr/J mice), CCL24 administration did not exacerbate high-cholesterol diet–induced atherosclerosis, confirming TLR4 dependence. TLR4 siRNA, MAPK pathway inhibitors, HuR/TTP/PRAT4A analysis, monocyte adhesion assay, Ldlr/J and LdlrTlr4 KO mice, western blot/qPCR American journal of translational research Medium 28078007
2007 GATA-1 transcription factor controls CCL24 production during eosinophilic differentiation: GATA-1 expression increases during ATRA-induced HT93 differentiation; GATA-1 siRNA knockdown reduces differentiation markers (CD11b, CCR3) and CCL24 production; GATA-1 overexpression enhances ATRA-induced differentiation and CCL24 production. CCR3+ cells produce more CCL24 than CCR3- cells. All-trans retinoic acid differentiation of HT93 cells, GATA-1 siRNA knockdown, GATA-1 overexpression clones, MACS enrichment of CCR3+ cells, ELISA for CCL24, flow cytometry Biological & pharmaceutical bulletin Medium 17917245
2019 Mast cell tryptase does not proteolytically cleave CCL24 (eotaxin-2), in contrast to eotaxin-1 (CCL11) and eotaxin-3 (CCL26), which are degraded by tryptase. This was confirmed by ELISA and PCR showing that tryptase reduced immunoreactivity of CCL11 and CCL26 but not CCL24 from conjunctival fibroblasts and from recombinant proteins. Tryptase proteolysis assay, ELISA, PCR, conjunctival fibroblast culture, recombinant protein substrates Japanese journal of ophthalmology Medium 30796548
2009 IL-13 directly and potently induces CCL24 (and CCL11) production from isolated oesophageal tissue rings via the IL-13Rα1/STAT6 signaling pathway (STAT6-deficient mice fail to produce CCL11 or CCL24 upon IL-13); oesophageal CCL11 expression temporally precedes CCL24 at high IL-13 concentrations. Oesophageal CCL24 production upon IL-13 stimulation is sufficient to promote eosinophil migration. Isolated oesophageal ring cultures (wild-type and STAT6 KO mice), IL-4/IL-13 stimulation, chemokine ELISA, IL-13Rα1/IL-13Rα2 expression analysis, eosinophil migration assay Clinical and experimental allergy High 20030665
2026 CCL24, transcriptionally repressed by EBF3, promotes M2-like macrophage polarization in lung adenocarcinoma; EBF3 overexpression reduces CCL24 production and M2 macrophage infiltration while increasing CD4+ and CD8+ T cell recruitment in vivo. Exogenous CCL24 rescues the tumor-suppressive and immune-modulatory effects of EBF3 in vivo, demonstrating that CCL24 is a direct mediator of EBF3-controlled immune remodeling. EBF3 overexpression/knockdown, syngeneic mouse tumor model, flow cytometry of immune infiltrates, conditioned medium macrophage polarization assay, CCL24 rescue experiment in vivo, Western blot (AKT/P38) Cellular oncology Medium 42018103
2026 CCL24 in peritoneal fibrosis is derived from macrophages and promotes mesothelial-to-mesenchymal transition (MMT) via the CCR3/P38 MAPK pathway. pMSC-derived exosomes delivering miR-320d suppress macrophage CCL24 synthesis via the KLF7/STAT3 pathway (miR-320d targets KLF7, which regulates STAT3 phosphorylation and CCL24 expression), ameliorating peritoneal fibrosis in a rat PD model. CCL24 KO/knockdown in macrophages, CCR3/P38 MAPK pathway inhibition, miR-320d mimic/exosome delivery, KLF7 target validation, STAT3 phosphorylation, in vivo rat PD fibrosis model, qRT-PCR, western blot, ELISA Scientific reports Medium 41781517

Source papers

Stage 0 corpus · 98 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 329 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 114 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 98 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 91 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 91 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 72 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
2024 Mechanical stiffness promotes skin fibrosis via Piezo1-Wnt2/Wnt11-CCL24 positive feedback loop. Cell death & disease 58 38267432
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 51 11286614
2017 Anserine/Carnosine Supplementation Suppresses the Expression of the Inflammatory Chemokine CCL24 in Peripheral Blood Mononuclear Cells from Elderly People. Nutrients 50 29088099
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
2020 A blocking monoclonal antibody to CCL24 alleviates liver fibrosis and inflammation in experimental models of liver damage. JHEP reports : innovation in hepatology 47 32039405
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 47 12915769
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 44 15695929
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
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 41 20236835
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 36 32051393
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
2023 CCL24 regulates biliary inflammation and fibrosis in primary sclerosing cholangitis. JCI insight 35 37345655
2011 Nasal lavage CCL24 levels correlate with eosinophils trafficking and symptoms in chronic sino-nasal eosinophilic inflammation. Rhinology 34 21743872
2014 Nasal fluid release of eotaxin-3 and eotaxin-2 in persistent sinonasal eosinophilic inflammation. International forum of allergy & rhinology 31 24989688
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
2015 A CCL24-dependent pathway augments eosinophilic airway inflammation in house dust mite-challenged Cd163(-/-) mice. Mucosal immunology 30 26376364
2013 Control of extravillous trophoblast function by the eotaxins CCL11, CCL24 and CCL26. Human reproduction (Oxford, England) 30 23477905
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
2021 CCL24 Signaling in the Tumor Microenvironment. Advances in experimental medicine and biology 19 34286443
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
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 18 37781651
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
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 12 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 12 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
2025 Macrophage-Derived CCL24 Promotes Cardiac Fibrosis Via Fibroblast CCR3. Circulation research 8 40955564
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
2023 CCL24, CXCL9 and CXCL10 are increased in synovial fluid in patients with juvenile idiopathic arthritis requiring advanced treatment. Rheumatology (Oxford, England) 6 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 6 37552963
2004 The chemokines CCL11, CCL20, CCL21, and CCL24 are preferentially expressed in polarized human secondary lymphoid follicles. The Journal of pathology 6 15376263
2014 All eotaxins CCL11, CCL24 and CCL26 are increased but to various extents in pulmonary tuberculosis patients. Clinical laboratory 5 24600981
2025 CCL24 and Fibrosis: A Narrative Review of Existing Evidence and Mechanisms. Cells 4 39851534
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
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
2022 Eotaxin-2 and eotaxin-3 in malaria exposure and pregnancy. Malaria journal 3 36380370
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
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
2026 mTORC1-Dependent Regulation of the CCL24-CCR3 Axis Controls Granuloma Formation and Maintenance in Sarcoidosis. Molecular and cellular biology 0 42246493
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

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