Affinage

CCL8

C-C motif chemokine 8 · UniProt P80075

Length
99 aa
Mass
11.2 kDa
Annotated
2026-06-09
97 papers in source corpus 47 papers cited in narrative 47 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

CCL8/MCP-2 is a secreted CC chemokine that orchestrates leukocyte recruitment across inflammation, infection, fibrosis, and tumor immunity by signaling through multiple G-protein-coupled receptors (PMID:1613466, PMID:7926371). Originally isolated from cytokine-stimulated osteosarcoma cells as a monocyte-specific chemoattractant structurally related to MCP-1, it also recruits CD4+ and CD8+ T lymphocytes, eosinophils, and basophils via pertussis toxin-sensitive, calcium-mobilizing signaling (PMID:1613466, PMID:7926371, PMID:7514401, PMID:7535823). CCL8 is functionally promiscuous, acting as an agonist at CCR1 and CCR2B (PMID:9115216), CCR5 (PMID:9790730), and CCR3 (PMID:29281969), with cross-desensitization establishing overlapping receptor usage shared with MCP-1, MCP-3, and RANTES on monocytes and eosinophils (PMID:7514401, PMID:7531149); in mice CCL8 uniquely activates CCR8 rather than CCR2, defining a CCL8-CCR8 axis that recruits inflammatory Th2 cells and drives eosinophilic skin inflammation (PMID:21217759). The mature CCL8(1-76) protein is proteolytically converted under synergistic IFN-γ plus IL-1β/TLR stimulation into CCL8(6-75), which loses agonist activity yet retains the ability to block CCR1/2/3/5, internalize CCR2, and antagonize ERK signaling and chemotaxis—an agonist-to-antagonist switch—while remaining resistant to MMP-9 processing (PMID:11023497, PMID:19224633). Its expression is induced by IFN-γ through a -340/-301 promoter element and JAK-STAT signaling (PMID:10496322, PMID:36672151), by NF-κB downstream of TLR2/TLR4 microbial sensing (PMID:23418602, PMID:36136589), and by chromatin and transcription factor regulators including ZEB1, STAT1, IRF1/JMJD1A, and CBX6/SMARCD1 (PMID:31263103, PMID:41720180, PMID:41779805, PMID:41219497), and is repressed transcriptionally by BLIMP1 and post-transcriptionally by miR-146a and miR-92a (PMID:24477914, PMID:20181935, PMID:25253336, PMID:29550454). Through these axes CCL8 recruits immunosuppressive and cytotoxic cells in disease: it drives macrophage and Treg recruitment to promote tumor growth and metastasis (PMID:27471618, PMID:32535027), mediates allograft rejection and acute GVHD (PMID:34808257, PMID:35973731), drives ERK1/2-dependent fibroblast collagen production in fibrosis (PMID:34391459), maintains spinal CCR5/ERK visceral pain signaling (PMID:29037608, PMID:29550454), negatively regulates myogenic muscle regeneration (PMID:39051762), and is produced by P16+ senescent fibroblasts and macrophages after myocardial infarction to recruit cytotoxic lymphocytes and impair cardiac repair (PMID:41766526).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1992 High

    Establishing that a distinct MCP-1-related CC chemokine existed answered whether a separate monocyte-selective chemoattractant could be biochemically purified and functionally defined.

    Evidence Protein purification, peptide sequencing, and chemotaxis from cytokine-stimulated osteosarcoma cells

    PMID:1613466

    Open questions at the time
    • No receptor identified
    • Cell selectivity beyond monocytes/neutrophils unexplored
  2. 1994 High

    Synthetic protein and cytokine-induction studies established CCL8's intrinsic chemotactic potency and that its regulation diverges from MCP-1, with IFN-γ as the superior inducer.

    Evidence Chemical synthesis, RIA, and cytokine stimulation of fibroblasts/leukocytes; T-cell chemotaxis with pertussis-toxin-sensitive Ca2+ flux

    PMID:7926371 PMID:8189067

    Open questions at the time
    • Specific receptor identity not resolved
    • Mechanism of differential regulation versus MCP-1 unknown
  3. 1995 High

    Cross-desensitization across leukocyte types resolved the question of CCL8 receptor usage, showing it shares receptor subgroups with MCP-1/MCP-3 and partially with RANTES, and can act as a functional inhibitor on basophils.

    Evidence Chemotaxis, Ca2+, mediator-release and radioligand competition on primary monocytes, eosinophils, and basophils

    PMID:7514401 PMID:7531149 PMID:7535823 PMID:7780043

    Open questions at the time
    • Receptor identities defined only by cross-competition, not molecular cloning
    • Basis of agonist versus inhibitor behavior unclear
  4. 1997 High

    Receptor-transfection binding assays identified the molecular receptors CCR1 and CCR2B, converting inferred receptor sharing into defined ligand-receptor pairs, alongside genomic cloning to chromosome 17q11.2.

    Evidence Radioiodinated ligand binding and chemotaxis on CCR1/CCR2B-transfected HEK293 cells; YAC contig cloning and Northern blot

    PMID:9115216 PMID:9119400

    Open questions at the time
    • Relative contribution of each receptor in vivo unknown
    • Tissue-specific receptor coupling not addressed
  5. 1998 High

    Demonstration of high-affinity CCR5 agonism resolved CCL8's primary receptor on activated T cells and revealed an antiviral capacity by blocking M-tropic HIV-1 entry.

    Evidence Radioligand binding, CCR5-transfectant chemotaxis, anti-CCR5 mAb blockade, and HIV-1 gp120 binding/infection inhibition

    PMID:9790730

    Open questions at the time
    • In vivo relevance of HIV inhibition untested
    • CCR5 signaling output not detailed
  6. 1999 High

    Promoter dissection answered how IFN-γ drives CCL8 transcription, mapping an inducible -340/-301 element and a basal -143/-73 region with IL-1β synergy.

    Evidence 5'-deletion luciferase reporters and EMSA in fibroblasts/osteosarcoma cells

    PMID:10496322

    Open questions at the time
    • Identity of the -340/-301 binding factors not established
    • STAT involvement inferred, not proven at this stage
  7. 2000 High

    Protease specificity testing established that CCL8 resists MMP-9 N-terminal processing, distinguishing its post-translational regulation from CXC chemokines.

    Evidence In vitro digestion with purified gelatinase B

    PMID:11023497

    Open questions at the time
    • Other processing proteases not surveyed here
    • Functional consequence of resistance unaddressed
  8. 2009 High

    Identification of the CCL8(6-75) cleavage product answered how CCL8 activity is switched off and inverted, converting an agonist into a multi-receptor antagonist that blocks ERK and chemotaxis.

    Evidence Protein purification, N-terminal sequencing, Ca2+ flux, chemotaxis, receptor internalization, and ERK assays

    PMID:19224633

    Open questions at the time
    • Identity of the processing protease not determined
    • In vivo abundance of antagonist form unknown
  9. 2010 Medium

    Discovery of miR-146a and miR-92a targeting CCL8 established post-transcriptional control during viral infection, complementing transcriptional regulation.

    Evidence miRNA overexpression with ELISA in HIV-infected microglia; HCMV latency secretome and miRNA analysis in myeloid progenitors

    PMID:20181935 PMID:25253336

    Open questions at the time
    • Direct 3'-UTR binding not fully validated in 2010 microglial study
    • Generalizability across cell types unknown
  10. 2011 High

    Knockout and adoptive-transfer studies defined the mouse CCL8-CCR8 axis as a Th2-recruitment pathway, revealing receptor specificity distinct from all other MCPs.

    Evidence Ccl8/Ccr8 knockout mice, atopic dermatitis model, adoptive transfer, flow cytometry

    PMID:21217759

    Open questions at the time
    • Human CCR8 agonism by CCL8 not equally established
    • Upstream inducers of CCL8 in skin not defined here
  11. 2014 High

    Genetic studies identified BLIMP1 as a direct transcriptional repressor of CCL8 and linked CCL8 to γδ T-cell-dependent antibacterial defense, defining a repression-controlled effector arm.

    Evidence Blimp1 conditional KO, Ccl8 KO, Listeria infection, chemotaxis, and γδ T-cell depletion

    PMID:24477914

    Open questions at the time
    • Direct BLIMP1 binding site on Ccl8 not mapped
    • Receptor mediating γδ recruitment not identified
  12. 2016 Medium

    Tumor studies established a CCL8/CCR5 axis recruiting regulatory T cells, framing CCL8 as a driver of an immunosuppressive metastatic niche.

    Evidence Ex vivo Treg migration, Maraviroc CCR5 blockade, and in vivo lung metastasis model

    PMID:27471618

    Open questions at the time
    • Maraviroc effects not CCL8-specific
    • Source-cell genetics not dissected
  13. 2020 High

    Macrophage-dependent tumor promotion by CCL8 was established genetically, showing CCL8 accelerates postpartum mammary tumorigenesis by recruiting M2 macrophages.

    Evidence Ccl8-deficient mice, tumor inoculation, and macrophage depletion rescue

    PMID:32535027

    Open questions at the time
    • Receptor on recruited macrophages not specified
    • Context dependence on involution unexplained mechanistically
  14. 2021 High

    Genetic and pharmacologic studies extended CCL8's pathogenic reach to acute GVHD mortality and to ERK1/2-driven fibroblast collagen production in fibrosis.

    Evidence Ccl8 KO with allogeneic BMT and survival; recombinant CCL8 on fibroblasts with anti-CCL8 in IgG4-related sialadenitis

    PMID:34391459 PMID:34808257

    Open questions at the time
    • GVHD effector receptor and cell type not defined
    • Fibroblast receptor mediating ERK activation not identified
  15. 2022 Medium

    Transplant and microbial studies clarified upstream control and downstream effects, showing donor macrophage Ccl8 drives CCR8+ T-cell graft infiltration and that iron amplifies TLR4/NF-κB-driven CCL8.

    Evidence Murine kidney transplant with CCL8-CCR8 blockade and macrophage depletion; iron/F. nucleatum macrophage NF-κB analysis

    PMID:35973731 PMID:36136589

    Open questions at the time
    • Long-term graft outcomes not assessed
    • Phosphatase target of iron not fully mapped
  16. 2023 Medium

    Multiple studies converged on CCL8/CCR5 and JAK-STAT-driven CCL8 as tumor- and inflammation-promoting axes, including a CCL8/CCR5/mTORC1 metastatic loop and IFN-γ/JAK-STAT fibroblast induction.

    Evidence Lactate/M2 macrophage colorectal model with CCR5 knockdown; IFN-γ/peficitinib fibroblast RNA-seq; MSC-podocyte VCAM-1-dependent co-culture

    PMID:36672151 PMID:37567910 PMID:38136340

    Open questions at the time
    • mTORC1 linkage to CCR5 mechanistically thin
    • Direct STAT binding to CCL8 promoter not shown in fibroblast study
  17. 2024 High

    In vivo gene editing established a non-immune role for CCL8 as an autocrine negative regulator of myogenic progenitor differentiation and muscle regeneration.

    Evidence AAV9 CRISPR depletion of Ccl8 in Pax7+/Myf5+/MyoD+ cells, barium chloride injury, and recombinant CCL8 rescue

    PMID:39051762

    Open questions at the time
    • Receptor mediating myogenic inhibition not identified
    • Downstream signaling in progenitors undefined
  18. 2025 Medium

    A wave of mechanistic studies defined transcriptional and chromatin regulators of CCL8 (STAT1/HSP90, IRF1/JMJD1A, CBX6/SMARCD1, USP18/SOCS1) and its roles in macrophage-mediated tumor immune evasion, cardiomyocyte inflammation, and asthma.

    Evidence Conditional KO mice, ChIP, knockdown/inhibitor studies, and CCL8-receptor-targeted DTCCL8 cytotoxin across cancer, AF, asthma, and intestinal models

    PMID:39774471 PMID:40545574 PMID:41219497 PMID:41354823 PMID:41408455 PMID:41720180 PMID:41779805

    Open questions at the time
    • Each regulatory axis from a single lab/context
    • Whether these converge on shared promoter elements unknown
  19. 2026 High

    Senescence-focused and therapy-context studies established CCL8 from P16+ cardiac cells as a driver of cytotoxic lymphocyte recruitment impairing repair, and chemotherapy-induced CCL8 as an NK-recruitment signal.

    Evidence p16-CreER dual-recombinase genetics with Ccl8 deletion and CD8 depletion in MI; MAPK-driven CCL8 chemotaxis with NK depletion in gastric cancer

    PMID:41766526 PMID:41843172

    Open questions at the time
    • Receptor on recruited cytotoxic lymphocytes not specified in cardiac model
    • Translational relevance to human MI untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved which receptor mediates CCL8's many non-canonical, often autocrine effects (myogenesis, fibroblast ERK activation, cardiac and GVHD pathology) and how its diverse transcriptional/chromatin regulators integrate at the promoter.
  • Receptor for muscle/fibroblast effects unknown
  • No structural model of CCL8-receptor complexes
  • In vivo abundance and role of the CCL8(6-75) antagonist undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 5 GO:0098772 molecular function regulator activity 2
Localization
GO:0005576 extracellular region 3
Pathway
R-HSA-1500931 Cell-Cell communication 4 R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 4
Partners
CCR1CCR2CCR3CCR5CCR8

Evidence

Reading pass · 47 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 CCL8/MCP-2 was isolated from cytokine-stimulated human osteosarcoma cells (MG-63), identified by peptide sequencing, and shown to specifically attract monocytes but not neutrophils in vitro and in vivo (intradermal injection in rabbits). It was classified as a CC chemokine with conserved cysteine residues, structurally related to MCP-1. Protein purification, peptide sequencing, chemotaxis assay (Boyden chamber), in vivo injection The Journal of experimental medicine High 1613466
1994 Synthetic CCL8/MCP-2 (76-residue protein) was chemotactic for monocytes at 1 nM; IFN-γ was identified as a superior inducer of MCP-2 (compared to IL-1β for MCP-1) in fibroblasts, while granulocytes were inefficient producers. Regulation of MCP-1 and MCP-2 expression was shown to be non-identical. Chemical synthesis, radioimmunoassay (RIA), cytokine stimulation of human fibroblasts and leukocytes Journal of immunology High 8189067
1994 CCL8/MCP-2 induced migration of human CD4+ and CD8+ T lymphocytes with a bimodal concentration dependence, elicited cytosolic Ca2+ increases blocked by pertussis toxin (indicating G-protein-coupled receptor involvement), and desensitization experiments showed MCP-1, MCP-2, and MCP-3 share receptors on T cells. Chemotaxis assay, intracellular Ca2+ measurement, pertussis toxin treatment, receptor desensitization, radioligand binding FASEB journal High 7926371
1994 CCL8/MCP-2 attracted human eosinophils (ED50 ~40 nM) and cross-desensitized eosinophil chemotactic responses to RANTES, indicating CCL8 and MCP-3 signal through the same receptor on eosinophils as RANTES. Boyden chamber eosinophil chemotaxis assay, cross-desensitization experiments Biochemical and biophysical research communications Medium 7514401
1995 CCL8/MCP-2 actions on human monocytes include bimodal migration, N-acetyl-β-D-glucosaminidase release, and Ca2+ transients. Cross-desensitization showed MCP-1, MCP-2, and MCP-3 share a receptor subgroup on monocytes distinct from the RANTES/MIP-1α/MIP-1β subgroup, though MCP-2 also partially interacts with the latter. Radiolabeled MCP-1 binding was competed by all MCPs; MCP-3 (but not MCP-1/MCP-2) fully displaced MIP-1α. Migration assay, exocytosis assay, Ca2+ measurement, cross-desensitization, radioligand binding competition European journal of immunology High 7531149
1995 CCL8/MCP-2 induced mediator release in human basophils (lower efficacy than MCP-1/MCP-3), Ca2+ transients, and chemotaxis in both basophils and eosinophils. Desensitization studies indicated MCP-2 interacts with receptors recognizing both MCP-1 and RANTES. In IL-3-untreated basophils, MCP-2 acted as a functional inhibitor of other CC chemokine actions. Mediator release assay, Ca2+ measurement, chemotaxis assay, cross-desensitization Journal of immunology High 7535823
1995 CCL8/MCP-2 and MCP-3 were chemically synthesized using Fmoc solid-phase chemistry, correctly folded with disulfide bridges in glutathione redox buffer, and shown to be chemotactic for monocytes at 7.5 ng/ml and 5 ng/ml respectively, equivalent to natural chemokines. Neither induced neutrophil chemotaxis. Solid-phase peptide synthesis, RP-HPLC purification, disulfide bridge formation, monocyte chemotaxis assay Cytokine High 7780043
1997 CCL8/MCP-2 uses CCR1 and CCR2B as functional receptors. 125I-MCP-2 bound to HEK293 cells transfected with CCR1 or CCR2B; binding was displaced by known CCR1/CCR2B ligands. Both CCR1- and CCR2B-transfected cells showed significant chemotactic migration in response to MCP-2. Radioiodinated ligand binding assay, receptor-transfected cell chemotaxis The Journal of biological chemistry High 9115216
1997 The human MCP-2/CCL8 gene (SCYA8) was cloned and localized to chromosome 17q11.2 within the CC chemokine gene contig. The gene shares a conserved intron-exon structure with MCP-1 and MCP-3 genes. MCP-2 mRNA (1.0 kb) was predominantly detected in small intestine, peripheral blood, heart, placenta, lung, and other tissues. YAC contig PCR cloning, genomic sequencing, Northern blot analysis Genomics High 9119400
1998 CCL8/MCP-2 binds CCR5 with high affinity and is a true CCR5 agonist, eliciting robust chemotaxis in CCR5 transfectants, cross-desensitization with RANTES on Ca2+ flux, and inhibiting M-tropic HIV-1 gp120 binding to CCR5 and HIV-1 infection of PBMCs. On activated CD3+/IL-2 T cells, CCL8-mediated chemotaxis was predominantly inhibited by anti-CCR5 mAb 2D7, establishing CCR5 as the primary receptor on these cells. Radioligand binding, chemotaxis of CCR5 transfectants, Ca2+ flux cross-desensitization, HIV-1 binding inhibition assay, anti-CCR5 mAb blocking Cellular immunology High 9790730
1999 The CCL8/MCP-2 gene promoter region between -340 and -301 (relative to transcription start site) is required for IFN-γ-induced transcription in fibroblasts and osteosarcoma cells. The region -143 to -73 (containing putative GATA-1, H-APF1, AP-1, and GAS elements) is important for basal transcription. IL-1β alone failed to induce expression, but synergized with IFN-γ in osteosarcoma cells. Transcription factors in nuclear extracts were shown to bind the -340/-301 region by EMSA. 5'-deletion mutagenesis, luciferase reporter assay, electromobility shift assay (EMSA) Journal of leukocyte biology High 10496322
2000 Neutrophil gelatinase B (MMP-9) does not digest CCL8/MCP-2 (or RANTES), in contrast to its processing of IL-8, CTAP-III, PF-4, and GRO-alpha. This establishes that CCL8 is resistant to MMP-9-mediated aminoterminal processing. In vitro protease digestion assay with purified gelatinase B Blood High 11023497
2003 The orphan mouse chemokine receptor L-CCR expressed in HEK293 cells showed pertussis toxin-sensitive chemotaxis and intracellular Ca2+ transients in response to CCL8 (and CCL2, CCL5, CCL7). Biotinylated CCL2 bound L-CCR-expressing cells, and L-CCR-GFP fusion protein localized to cell membranes. Receptor transfection in HEK293, chemotaxis assay, Ca2+ measurement, pertussis toxin treatment, biotinylated ligand binding, GFP fusion protein localization Journal of leukocyte biology Medium 12885941
2005 TRAIL pretreatment of endothelial cells abrogated TNF-α-mediated upregulation of CCL8 and CXCL10 mRNA, as identified by cDNA microarray. Addition of recombinant CCL8 plus CXCL10 to endothelial cultures completely restored the proadhesive activity of TNF-α, demonstrating that CCL8 contributes to leukocyte/endothelial adhesion. Both TRAIL-R1 and TRAIL-R2 contributed to this chemokine modulation. cDNA microarray, qPCR, recombinant protein rescue experiment, agonistic anti-TRAIL receptor antibodies Blood Medium 15644410
2009 Intact CCL8/MCP-2(1-76) produced by fibroblasts is processed into CCL8(6-75) under synergistic IFN-γ + IL-1β (or TLR ligand) stimulation. The truncated isoform CCL8(6-75) lacked chemotactic activity for monocytes and had severely reduced capacity to increase intracellular Ca2+ via CCR1, CCR2, CCR3, and CCR5. However, CCL8(6-75) still blocked these receptors, induced CCR2 internalization, inhibited MCP-1/CCL2 and MCP-2/CCL8 ERK signaling, and antagonized chemotactic activity of several CCR2 ligands. Protein purification, N-terminal sequencing, Ca2+ flux assay, chemotaxis assay, receptor internalization assay, ERK phosphorylation assay European journal of immunology High 19224633
2010 CCL8/MCP-2 is a direct target of miR-146a in HIV-1-infected human microglial cells. Overexpression of miR-146a prevented HIV-induced secretion of MCP-2. In HIV-encephalitis brain samples, decreased MCP-2 levels coincided with increased miR-146a, suggesting post-transcriptional regulation of CCL8 by miR-146a during chronic neuroinflammation. miRNA overexpression, ELISA for MCP-2 secretion, HIV-1 infection of primary microglial cells, brain tissue analysis FASEB journal Medium 20181935
2010 Stromal cell-derived CCL8 cooperated with CXCL12 to attract hematopoietic progenitors capable of differentiating into regulatory dendritic cells. Leishmania donovani infection of murine bone marrow stromal cells enhanced CCL8 production and their capacity to support regulatory DC development. In experimental visceral leishmaniasis, CCL8 production was induced in splenic stromal cells. Hematopoietic progenitor migration assay, stromal cell infection, in vivo murine leishmaniasis model, DC differentiation assay Journal of immunology Medium 20624948
2011 Mouse CCL8 is a CCR8 agonist but not a CCR2 agonist, distinguishing it from all other MCP chemokines. CCL8-CCR8 signaling defines a population of highly differentiated CCR8-expressing inflammatory Th2 cells enriched for IL-5. Ccr8- and Ccl8-deficient mice had markedly less eosinophilic inflammation in a chronic atopic dermatitis model. Adoptive transfer studies established CCR8 as a key regulator of Th2 cell recruitment into allergen-inflamed skin. Receptor binding/signaling assays, Ccr8/Ccl8 knockout mice, chronic atopic dermatitis model, adoptive transfer studies, flow cytometry Nature immunology High 21217759
2013 Mycobacterium bovis BCG and M. tuberculosis H37Rv infection induced CCL8/MCP-2 production in macrophage cell lines and primary macrophages through TLR2/PI3K/Akt and p38 signaling pathways. CCR5 (primary receptor for MCP-2/CCL8) was predominantly expressed on pleural CD4+ T lymphocytes in TB patients, suggesting CCL8 mediates T lymphocyte recruitment in pleural TB. Mycobacterial infection of macrophages, signaling pathway inhibitors, qPCR, protein array, flow cytometry on patient samples PloS one Medium 23418602
2014 BLIMP1 is a direct transcriptional repressor of CCL8 in macrophages. BLIMP1-deficient macrophages expressed elevated Ccl8, and Blimp1 CKO mice had higher circulating CCL8 and increased neutrophils, promoting antibacterial responses. CCL8 was chemotactic for γ/δ T cells enriched for IL-17F, and CCL8-mediated clearance of Listeria monocytogenes was dependent on γ/δ T cells. CCL8 failed to recruit neutrophils directly. Conditional knockout mice (Blimp1 CKO in myeloid cells), transcriptome analysis, Ccl8 knockout mice, Listeria infection model, chemotaxis assay, γ/δ T cell depletion Journal of immunology High 24477914
2014 LAcmvIL-10 (HCMV latency-associated viral IL-10) is responsible for increased CCL8 secretion from latently infected myeloid progenitors. This occurs through LAcmvIL-10-mediated suppression of cellular microRNA hsa-miR-92a, which directly targets CCL8. Downregulation of hsa-miR-92a thus upregulates CCL8 during HCMV latency. Latent infection of primary myeloid progenitors, miRNA expression analysis, secretome analysis Journal of virology Medium 25253336
2016 CCL8 is produced by F4/80+ macrophages in the lungs of mice with metastatic primary tumors and drives CCR5-dependent Treg migration. Ex vivo Treg migration toward CCL8 was reduced by CCR5 inhibitor Maraviroc. Maraviroc treatment reduced CCR5+ Tregs and metastatic tumor burden in lungs, establishing a CCL8/CCR5 signaling axis for Treg recruitment. Ex vivo migration assay, flow cytometry, Maraviroc treatment, immunofluorescence, in vivo metastasis model Oncoimmunology Medium 27471618
2017 Recombinant CCL8 produced in E. coli binds CCR3 with a dissociation equilibrium constant (KD) of 1.2 × 10-7 M as measured by quartz crystal microbalance. CCL8 induced internalization of CCR3 in vivo within 1 hour at 100 nM and elicited weaker chemotactic effects in CCR3-expressing cells compared to CCL11 and CCL24. Recombinant protein production, quartz crystal microbalance binding assay, receptor internalization assay, chemotaxis assay BMC immunology Medium 29281969
2017 CCL8 expression in spinal neurons (co-localized with NeuN marker) was upregulated following TNBS-induced colonic inflammation. Intrathecal CCL8 neutralizing antibody or CCR5 antagonist DAPTA dose-dependently suppressed TNBS-evoked visceral hyperalgesia and spinal ERK activation, establishing a CCL8/CCR5/ERK pathway in spinal cord visceral pain maintenance. TNBS colitis model, immunohistochemistry, qPCR/Western blot, intrathecal antibody/antagonist injection, colorectal distension pain assay, ERK phosphorylation analysis Brain research bulletin Medium 29037608
2018 miR-146a-5p directly targets the 3'-UTR of CCL8, as confirmed by dual-luciferase reporter assay. In Neuro-2a cells, TNF-α-induced CCL8 upregulation was decreased by miR-146a-5p mimic. Intrathecal miR-146a-5p agomir reduced CCL8 expression and relieved visceral pain in colitis mice; intrathecal antagomir upregulated CCL8 and induced pain hypersensitivity that was partially rescued by CCL8 neutralization. Dual-luciferase reporter assay, miRNA mimic/inhibitor transfection, intrathecal injection, TNBS colitis model, pain threshold measurement Brain research bulletin High 29550454
2019 Hypoxia-induced ZEB1 activates CCL8 transcription in cervical cancer cells, which attracts macrophages via the CCR2-NF-κB pathway. ZEB1 knockdown altered expression of multiple chemokines with CCL8 being most affected, and CCL8-dependent macrophage migration was demonstrated in vitro. Hypoxia treatment, ZEB1 knockdown/overexpression, chemokine expression profiling, macrophage migration assay, CCR2-NF-κB pathway analysis Cell death & disease Medium 31263103
2019 miR-345-5p directly targets CCL8 (confirmed by luciferase assay) and inversely correlates with CCL8 expression in PDAC samples. CCL8 activates the NF-κB signaling pathway to promote proliferation and invasiveness of pancreatic cancer cells. Luciferase reporter assay, miRNA overexpression, Western blot for NF-κB pathway, Transwell invasion assay Biomedicine & pharmacotherapy Medium 30841468
2020 CCL8 promotes migratory ability of endometrial epithelial and stromal cells and increases proliferation, migration, and tube formation of endothelial cells through CCR1. CCR1, overexpressed in ectopic endometrium and co-localized with blood vessels, when inhibited suppressed endometriosis development and angiogenesis in vivo. CCL8 was upregulated in mast cells when co-cultured with endometrial cells. Co-culture system, Transwell migration assay, CCK-8 proliferation assay, tube formation assay, CCR1 inhibition in vivo mouse model Biomedicine & pharmacotherapy Medium 32768961
2020 CCL8 is highly expressed during mammary gland involution and enhances infiltration of M2 subtype macrophages at the second phase of involution. In Ccl8-deficient animals, CCL8 accelerated tumor onset during involution but not in nulliparous animals. Macrophage depletion abolished the tumor-promoting effect of CCL8, establishing that CCL8 promotes postpartum breast cancer by recruiting M2 macrophages. Ccl8-deficient mice, cancer cell inoculation studies, macrophage depletion, immunohistochemistry iScience High 32535027
2021 CCL8 from endothelial colony forming cells (ECFCs) induces IL-8 secretion from TNBC cells via c-Jun as a transcription factor. A positive feedback loop between CCL8 and IL-8 contributes to invasion, migration, MMP-2 secretion, and angiogenesis. CCL8 was crucial for ECFC-induced invasion of MDA-MB-231 cells. Indirect co-culture, cytokine antibody array, RT-PCR, siRNA knockdown, xenograft model, transcription factor identification Oncogene Medium 33833397
2021 CCL8 plays a major role in acute GVHD pathogenesis. CCL8-knockout mice showed markedly reduced mortality (23.4% vs. 90% in wild-type) and attenuated liver dysfunction after allogeneic bone marrow transplantation. CCL8 deficiency was associated with a surge in plasma IL-6 in allograft recipients, suggesting CCL8 involvement in an IL-6 signaling cascade during aGVHD. CCL8 knockout mice, allogeneic bone marrow transplantation, survival analysis, plasma cytokine measurement, histopathology Experimental hematology High 34808257
2022 Iron augmented Fusobacterium nucleatum-induced CCL8 expression in macrophages via TLR4/NF-κB signaling. Mechanistically, iron attenuated inhibitory phosphorylation of NF-κB p65 by activating serine/threonine phosphatases, thereby augmenting tumor-promoting chemokine production. qRT-PCR, Western blot, NF-κB signaling analysis, iron deficiency/supplementation experiments JCI insight Medium 36136589
2022 Donor kidney resident macrophages rapidly induced Ccl8 expression within 3 days post-transplant, which promoted recipient monocyte graft infiltration and their differentiation to resident macrophages, which in turn also expressed Ccl8. CCL8-CCR8 signaling then enhanced CCR8+ T cell (CD4, CD8, γδ) infiltration. Blocking CCL8-CCR8 or depleting donor kidney resident macrophages significantly inhibited early allograft immune cell infiltration and improved short-term function. Allogeneic murine kidney transplant model, CCL8-CCR8 blockade, macrophage depletion, flow cytometry, single-cell analysis Journal of the American Society of Nephrology High 35973731
2023 Lactate induced M2 macrophage polarization via AKT/ERK signaling pathway; M2 macrophages subsequently secreted CCL8 which facilitated colorectal cancer cell proliferation and metastasis by activating the CCL8/CCR5/mTORC1 axis. CCR5 antagonism or knockdown inhibited this protumorigenic effect. qRT-PCR, Western blot, RNA-seq, wound healing assay, colony formation assay, CCR5 knockdown/antagonist, allograft mouse model Cancers Medium 38136340
2023 IFN-γ stimulation of fibroblasts via JAK-STAT signaling upregulated CCL2 and CCL8 expression. CCL2 addition to naïve T cell polarization promoted type 2 cytokine secretion. JAK inhibitor peficitinib abrogated IFN-γ-induced CCL2 and CCL8 upregulation in fibroblasts. RNA sequencing of vitiligo mouse model fibroblasts, JAK inhibitor treatment, qPCR, Western blot, T cell polarization assay, flow cytometry Cells Medium 36672151
2023 MSCs enhanced CCL8 expression by podocytes in a contact-dependent manner (blocked by anti-VCAM-1 antibody, shown by transwell assay). Conversely, podocyte-derived CCL8 potentiated immunosuppressive activity of MSCs (increased IL-10, IDO, TGF-β1, iNOS production and stronger inhibition of IFN-γ by T cells). Co-culture, transwell assay, anti-VCAM-1 antibody blocking, qPCR/Western blot, T cell suppression assay Scientific reports Medium 37567910
2024 Muscle cell-derived Ccl8 (from Pax7+, Myf5+, or MyoD+ myogenic progenitor cells) negatively regulates skeletal muscle regeneration. CRISPR-based depletion of Ccl8 in Pax7+ MPCs accelerated muscle regeneration after injury in both young and middle-aged mice. Intramuscular administration of recombinant Ccl8 reversed this accelerated regeneration phenotype, establishing Ccl8 as a negative regulator of myogenic differentiation initiation. Ccl8 knockdown in C2C12 myoblasts, AAV9-delivered sgRNA/Cas9 in vivo gene editing in Pax7+/Myf5+/MyoD+ cells, barium chloride injury model, recombinant CCL8 rescue FASEB journal High 39051762
2025 CCL8 is identified as a critical mediator downstream of GAS6/AXL/MERTK signaling in tumor-associated macrophages (Reg-TAMs) that facilitates immune escape of tumor-initiating cells primarily by inhibiting Treg infiltration into the tumor. AXL/MERTK inhibition reactivated antitumor immunity and sensitized tumor cells to anti-PD-1 treatment. scRNA-seq, lineage tracing, chemical inhibitors, Axl/Mertk conditional double-KO mice, anti-PD-1 combination studies The Journal of clinical investigation Medium 39774471
2025 USP18 stabilizes SOCS1 by inhibiting its ubiquitination and degradation, leading to reduced CCL8 production in AT2 cells through the ERK-STAT3 signaling pathway. USP18 deficiency increased CCL8 in AT2 cells, recruiting Th2 cells and eosinophils to exacerbate allergic asthma. CCL8 knockdown in AT2 cells of USP18 KO mice alleviated asthma symptoms. USP18 KO mice, AT2 cell-specific CCL8 knockdown, exogenous CCL8 treatment, SOCS1 ubiquitination assay, ERK-STAT3 pathway analysis Respiratory research Medium 41354823
2025 DTCCL8, a chimeric diphtheria toxin-CCL8 cytotoxic peptide, was developed to ablate cells expressing CCL8 receptors (particularly CCR5). Its specificity was confirmed in vitro by testing cytotoxic activity on CCR5-overexpressing breast cancer cells and by neutralizing anti-CCL8 antibody. In vivo, DTCCL8 showed anticancer activity in polyoma middle T oncogene-driven mouse breast cancers. Chimeric protein construction, in vitro cytotoxicity on CCR5-expressing cells, anti-CCL8 neutralizing antibody, in vivo mouse breast cancer model Molecular oncology Medium 40545574
2025 HSP90 interacts with transcription factor STAT1 and stabilizes its expression, driving CCL8 expression in atrial cardiomyocytes. CCL8 mediates macrophage recruitment and local atrial inflammation in hypertension-induced atrial fibrillation. STAT1 knockdown attenuated CCL8 upregulation and the inflammatory cascade. RNA sequencing, AngII-induced AF mouse model, HSP90 inhibitor (17AAG), STAT1 knockdown, Western blot, co-IP (HSP90-STAT1 interaction inferred) Life sciences Medium 41720180
2025 JMJD1A (KDM3A) promotes CCL8 expression in colonic epithelial cells by demethylating H3K9me2 on both the IRF1 promoter (cooperating with STAT1 to upregulate IRF1) and the CCL8 promoter directly (cooperating with IRF1). CCL8 mediates recruitment of macrophages and CD4+ T cells, and JMJD1A-/- mice showed impaired CCL8 induction and reduced immune cell recruitment after C. rodentium infection. JMJD1A knockout mice, C. rodentium infection model, ChIP for H3K9me2, promoter analysis, flow cytometry for immune cell recruitment PLoS pathogens Medium 41779805
2025 CBX6 promotes CCL8 expression in esophageal squamous cell carcinoma cells through SMARCD1-mediated chromatin remodeling. CBX6 regulated SMARCD1 expression to modulate chromatin remodeling, thereby promoting CCL8 transcription. CCL8 secretion contributed to CD8+ T cell exhaustion and reduced cytotoxicity. Cbx6 knockdown, SMARCD1 overexpression, co-culture with CD8+ T cells, in vivo tumorigenesis model, tissue microarray Cell biology and toxicology Medium 41219497
2026 P16+ fibroblasts and macrophages after myocardial infarction are the main sources of CCL8 in the heart. CCL8 blockade or genetic deletion of Ccl8 in P16+ cells reduced infiltration of cytotoxic lymphocytes (CD8+ T cells and NK cells), decreased cardiomyocyte apoptosis, and enhanced cardiac repair. Ablation of P16+ fibroblasts (but not macrophages) diminished fibrosis. p16-CreER reporter mice, dasatinib/quercetin senolytic treatment, bulk and scRNA-seq of P16+ cells, CCL8 neutralization, Ccl8 deletion in P16+ cells, CD8+ T cell depletion, dual-recombinase intersectional genetics Circulation High 41766526
2021 Recombinant mouse CCL8 stimulation of NIH/3T3 fibroblasts significantly increased collagen expression and ERK1/2 phosphorylation, suggesting CCL8 drives fibrosis via ERK1/2 phosphorylation. Anti-CCL8 neutralizing antibody improved focus and fibrosis scores in an IgG4-related sialadenitis mouse model (LAT Y136F knockin mice). Recombinant CCL8 stimulation of fibroblasts, Western blot for ERK1/2 phosphorylation, collagen expression assay, anti-CCL8 antibody treatment in vivo Arthritis research & therapy Medium 34391459
2025 CCL8 induced M1 macrophage polarization in THP1-derived macrophages; conditioned medium from these macrophages suppressed ovarian cancer cell proliferation, migration, invasion, and EMT. Mechanistically, CCL8-induced macrophages promoted apoptosis in OC cells via activation of the NF-κB p65 pathway (increased Bax and Caspase3), which was reversed by p65 inhibition. Macrophage polarization assay, conditioned medium transfer, NF-κB inhibition, Western blot for apoptosis markers, proliferation/invasion assays Scientific reports Medium 41408455
2026 Neoadjuvant chemotherapy activates the MAPK pathway in gastric cancer cells, inducing CCL8 secretion which facilitates NK cell recruitment. In vitro, NACT-treated tumor cells showed enhanced chemotactic effects on NK92 cells, and NACT-induced CCL8 was identified as the mechanistic driver of NK cell recruitment. In vitro NACT treatment, chemotaxis assay, MAPK pathway analysis, in vivo NK cell depletion Cancer immunology, immunotherapy Medium 41843172

Source papers

Stage 0 corpus · 97 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 Neutrophil gelatinase B potentiates interleukin-8 tenfold by aminoterminal processing, whereas it degrades CTAP-III, PF-4, and GRO-alpha and leaves RANTES and MCP-2 intact. Blood 546 11023497
1992 Structural and functional identification of two human, tumor-derived monocyte chemotactic proteins (MCP-2 and MCP-3) belonging to the chemokine family. The Journal of experimental medicine 360 1613466
1994 Monocyte chemotactic proteins MCP-1, MCP-2, and MCP-3 are major attractants for human CD4+ and CD8+ T lymphocytes. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 309 7926371
1995 Actions of the chemotactic cytokines MCP-1, MCP-2, MCP-3, RANTES, MIP-1 alpha and MIP-1 beta on human monocytes. European journal of immunology 308 7531149
1998 MCP-1, MCP-2 and MCP-3 expression in multiple sclerosis lesions: an immunohistochemical and in situ hybridization study. Journal of neuroimmunology 307 9655469
2011 Mouse CCL8, a CCR8 agonist, promotes atopic dermatitis by recruiting IL-5+ T(H)2 cells. Nature immunology 261 21217759
2008 Evaluating the potential of IP-10 and MCP-2 as biomarkers for the diagnosis of tuberculosis. The European respiratory journal 156 18684849
2003 Association of genetic variants of the chemokine receptor CCR5 and its ligands, RANTES and MCP-2, with outcome of HCV infection. Hepatology (Baltimore, Md.) 153 14647058
1999 Expression of monocyte chemotactic protein (MCP)-1, MCP-2, and MCP-3 by human airway smooth-muscle cells. Modulation by corticosteroids and T-helper 2 cytokines. American journal of respiratory cell and molecular biology 122 10502563
1997 Monocyte chemotactic protein-2 (MCP-2) uses CCR1 and CCR2B as its functional receptors. The Journal of biological chemistry 121 9115216
2019 Hypoxia-induced ZEB1 promotes cervical cancer progression via CCL8-dependent tumour-associated macrophage recruitment. Cell death & disease 112 31263103
2010 CCL8/MCP-2 is a target for mir-146a in HIV-1-infected human microglial cells. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 108 20181935
1994 Induction of monocyte chemotactic proteins MCP-1 and MCP-2 in human fibroblasts and leukocytes by cytokines and cytokine inducers. Chemical synthesis of MCP-2 and development of a specific RIA. Journal of immunology (Baltimore, Md. : 1950) 107 8189067
2009 IP-10, MCP-1, MCP-2, MCP-3, and IL-1RA hold promise as biomarkers for infection with M. tuberculosis in a whole blood based T-cell assay. BMC research notes 100 19193208
2005 TRAIL counteracts the proadhesive activity of inflammatory cytokines in endothelial cells by down-modulating CCL8 and CXCL10 chemokine expression and release. Blood 97 15644410
2016 Maraviroc decreases CCL8-mediated migration of CCR5(+) regulatory T cells and reduces metastatic tumor growth in the lungs. Oncoimmunology 94 27471618
1995 Monocyte chemotactic protein MCP-2 activates human basophil and eosinophil leukocytes similar to MCP-3. Journal of immunology (Baltimore, Md. : 1950) 86 7535823
1994 Human monocyte chemotactic proteins-2 and 3 (MCP-2 and MCP-3) attract human eosinophils and desensitize the chemotactic responses towards RANTES. Biochemical and biophysical research communications 79 7514401
2016 A CCL8 gradient drives breast cancer cell dissemination. Oncogene 75 27181207
1998 CCR5 has an expanded ligand-binding repertoire and is the primary receptor used by MCP-2 on activated T cells. Cellular immunology 65 9790730
2008 CCL8 is a potential molecular candidate for the diagnosis of graft-versus-host disease. Blood 61 18256320
2009 Synergistic up-regulation of MCP-2/CCL8 activity is counteracted by chemokine cleavage, limiting its inflammatory and anti-tumoral effects. European journal of immunology 60 19224633
2014 Latency-associated viral interleukin-10 (IL-10) encoded by human cytomegalovirus modulates cellular IL-10 and CCL8 Secretion during latent infection through changes in the cellular microRNA hsa-miR-92a. Journal of virology 58 25253336
2019 MiR-345-5p functions as a tumor suppressor in pancreatic cancer by directly targeting CCL8. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 55 30841468
2017 Gene profile of fibroblasts identify relation of CCL8 with idiopathic pulmonary fibrosis. Respiratory research 43 28057004
2015 The importance of microenvironment: the role of CCL8 in metastasis formation of melanoma. Oncotarget 43 26320180
2003 Expression of L-CCR in HEK 293 cells reveals functional responses to CCL2, CCL5, CCL7, and CCL8. Journal of leukocyte biology 40 12885941
2020 Possible involvement of crosstalk between endometrial cells and mast cells in the development of endometriosis via CCL8/CCR1. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 38 32768961
1985 Newborn rabbit alveolar macrophages are deficient in two microbicidal cationic peptides, MCP-1 and MCP-2. The American review of respiratory disease 36 4051325
2020 CCL8 Promotes Postpartum Breast Cancer by Recruiting M2 Macrophages. iScience 34 32535027
1997 The human MCP-2 gene (SCYA8): cloning, sequence analysis, tissue expression, and assignment to the CC chemokine gene contig on chromosome 17q11.2. Genomics 34 9119400
1995 Chemical synthesis, purification and folding of the human monocyte chemotactic proteins MCP-2 and MCP-3 into biologically active chemokines. Cytokine 34 7780043
2006 Cytokine and chemokine transcription profile during Mycoplasma pulmonis infection in susceptible and resistant strains of mice: macrophage inflammatory protein 1beta (CCL4) and monocyte chemoattractant protein 2 (CCL8) and accumulation of CCR5+ Th cells. Infection and immunity 33 16988274
2017 Functional expression of CCL8 and its interaction with chemokine receptor CCR3. BMC immunology 32 29281969
1997 Induction of gelatinase B and MCP-2 in baboons during sublethal and lethal bacteraemia. Cytokine 32 9199875
1985 Cytotoxicity of rabbit macrophage peptides MCP-1 and MCP-2 for mouse tumor cells. Antimicrobial agents and chemotherapy 31 4091528
2023 Pathogenic Th2 Cytokine Profile Skewing by IFN-γ-Responding Vitiligo Fibroblasts via CCL2/CCL8. Cells 30 36672151
2017 Chemokine CCL8 and its receptor CCR5 in the spinal cord are involved in visceral pain induced by experimental colitis in mice. Brain research bulletin 30 29037608
2014 The transcriptional repressor BLIMP1 curbs host defenses by suppressing expression of the chemokine CCL8. Journal of immunology (Baltimore, Md. : 1950) 30 24477914
2013 Induction of CCL8/MCP-2 by mycobacteria through the activation of TLR2/PI3K/Akt signaling pathway. PloS one 29 23418602
2014 Allergic airway inflammation decreases lung bacterial burden following acute Klebsiella pneumoniae infection in a neutrophil- and CCL8-dependent manner. Infection and immunity 28 24958709
2008 Oncostatin M-induced and constitutive activation of the JAK2/STAT5/CIS pathway suppresses CCL1, but not CCL7 and CCL8, chemokine expression. Journal of immunology (Baltimore, Md. : 1950) 28 18981157
2023 Lactate-Induced CCL8 in Tumor-Associated Macrophages Accelerates the Progression of Colorectal Cancer through the CCL8/CCR5/mTORC1 Axis. Cancers 27 38136340
2022 Iron accelerates Fusobacterium nucleatum-induced CCL8 expression in macrophages and is associated with colorectal cancer progression. JCI insight 25 36136589
2018 Nicaraven reduces cancer metastasis to irradiated lungs by decreasing CCL8 and macrophage recruitment. Cancer letters 25 29339207
2019 CCL8 enhances sensitivity of cutaneous squamous cell carcinoma to photodynamic therapy by recruiting M1 macrophages. Photodiagnosis and photodynamic therapy 24 30902794
2000 Cloning of equine chemokines eotaxin, monocyte chemoattractant protein (MCP)-1, MCP-2 and MCP-4, mRNA expression in tissues and induction by IL-4 in dermal fibroblasts. Veterinary immunology and immunopathology 24 11044560
2013 Monitoring of TNFR1, IL-2Rα, HGF, CCL8, IL-8 and IL-12p70 following HSCT and their role as GVHD biomarkers in paediatric patients. Bone marrow transplantation 23 23584443
2010 Stromal cell-derived CXCL12 and CCL8 cooperate to support increased development of regulatory dendritic cells following Leishmania infection. Journal of immunology (Baltimore, Md. : 1950) 23 20624948
2024 Single-cell RNA sequencing reveals recruitment of the M2-like CCL8high macrophages in Lewis lung carcinoma-bearing mice following hypofractionated radiotherapy. Journal of translational medicine 21 38528587
2022 Blocking CCL8-CCR8-Mediated Early Allograft Inflammation Improves Kidney Transplant Function. Journal of the American Society of Nephrology : JASN 21 35973731
2021 CCL8 mediates crosstalk between endothelial colony forming cells and triple-negative breast cancer cells through IL-8, aggravating invasion and tumorigenicity. Oncogene 21 33833397
2001 Expression of the chemokines, monocyte chemotactic protein (MCP)-1 and MCP-2 in endometrium of normal women and Norplant users, does not support a central role in macrophage infiltration into endometrium. Journal of reproductive immunology 21 11164897
2018 MicroRNA-146a-5p attenuates visceral hypersensitivity through targeting chemokine CCL8 in the spinal cord in a mouse model of colitis. Brain research bulletin 17 29550454
2015 CCL8 and the Immune Control of Cytomegalovirus in Organ Transplant Recipients. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 17 25764912
2020 CaSR Antagonist (Calcilytic) NPS 2143 Hinders the Release of Neuroinflammatory IL-6, Soluble ICAM-1, RANTES, and MCP-2 from Aβ-Exposed Human Cortical Astrocytes. Cells 14 32498476
2019 MicroRNA-181 inhibits glioblastoma cell growth by directly targeting CCL8. Oncology letters 14 31423262
2012 Pseudogenization of the MCP-2/CCL8 chemokine gene in European rabbit (genus Oryctolagus), but not in species of Cottontail rabbit (Sylvilagus) and Hare (Lepus). BMC genetics 14 22894773
2011 Early expression of plasma CCL8 closely correlates with survival rate of acute graft-vs.-host disease in mice. Experimental hematology 14 21782767
1999 Transcriptional control of the human MCP-2 gene promoter by IFN-gamma and IL-1beta in connective tissue cells. Journal of leukocyte biology 14 10496322
2025 Insights on the role of the chemokine CCL8 in pathology. Cellular signalling 12 40541814
2022 Beneficial effects of CCL8 inhibition at lipopolysaccharide-induced lung injury. iScience 12 36404927
2021 Pathogenic roles and therapeutic potential of the CCL8-CCR8 axis in a murine model of IgG4-related sialadenitis. Arthritis research & therapy 12 34391459
1994 Porcine luteal cells express monocyte chemoattractant protein-2 (MCP-2): analysis by cDNA cloning and northern analysis. Biochemical and biophysical research communications 12 7999015
2020 Evaluation of the inflammatory markers CCL8, CXCL5, and LIF in patients with anastomotic leakage after colorectal cancer surgery. International journal of colorectal disease 9 32307587
2009 Upregulation of plasma CCL8 in mouse model of graft-vs-host disease. Experimental hematology 9 19302923
2012 Janus kinase 2 and signal transducer and activator of transcription 3 activation is not essential for CCL3-, CCL5- or CCL8-induced chemotaxis. Cell biochemistry and function 8 22987449
2023 Mesenchymal stem cells enhance CCL8 expression by podocytes in lupus-prone MRL.Faslpr mice. Scientific reports 7 37567910
2016 Adaptive Gene Loss? Tracing Back the Pseudogenization of the Rabbit CCL8 Chemokine. Journal of molecular evolution 7 27306379
2025 Tumor-initiating cells escape tumor immunity via CCL8 from tumor-associated macrophages in mice. The Journal of clinical investigation 6 39774471
2021 Serum levels of NLRC4 and MCP-2/CCL8 in patients with active Crohn's disease. PloS one 6 34788319
2021 CCL8 deficiency in the host abrogates early mortality of acute graft-versus-host disease in mice with dysregulated IL-6 expression. Experimental hematology 6 34808257
2009 CCL8/MCP-2 association analysis in patients with Alzheimer's disease and frontotemporal lobar degeneration. Journal of neurology 6 19415413
2024 Muscle cell-derived Ccl8 is a negative regulator of skeletal muscle regeneration. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 5 39051762
2019 Diagnostic Accuracy of Monocyte Chemotactic Protein (MCP)-2 as Biomarker in Response to PE35/PPE68 Proteins: A Promising Diagnostic Method for the Discrimination of Active and Latent Tuberculosis. Protein and peptide letters 5 30663558
2025 Chimeric diphtheria toxin-CCL8 cytotoxic peptide for breast cancer management. Molecular oncology 4 40545574
2023 Identification of potent anti-Candida metabolites produced by the soft coral associated Streptomyces sp. HC14 using chemoinformatics. Scientific reports 4 37532728
2022 Dexamethasone attenuated thoracic aortic aneurysm and dissection in vascular smooth muscle cell Tgfbr2-disrupted mice with CCL8 suppression. Experimental physiology 4 35344629
2021 Association between the Genetic Polymorphisms of CCL2, CCL5, CCL8, CCR2, and CCR5 with Chronic Hepatitis C Virus Infection in the Chinese Han Population. Immunological investigations 4 33902378
2023 CCL2, CCL8, CXCL12 chemokines in resectable non-small cell lung cancer (NSCLC). Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia 3 36628560
2020 Silencing CCL8 inhibited the proliferation and migration of PDGF-BB-stimulated human aortic smooth muscle cells. Bioscience, biotechnology, and biochemistry 3 32432500
2025 Targeting NLRP1-CCL8 axis in the leukaemic niche suppresses AML via inhibition of PI3K-AKT signalling. British journal of haematology 2 40685774
2025 Spatiotemporal mapping reveals Ccl8hi macrophages as key drivers of testicular inflammaging. Clinical and translational medicine 2 41251087
2024 Evaluation of serum MIP-1β and MCP-2 levels in major depressive disorder: A case-control study. PloS one 2 38889138
2021 Revisiting CCL-type chemokines in breast cancer and its milieu: prominent targetable chemokines, CCL8 and CCL21. Bioscience reports 2 34160019
2025 Checkpoint Blockade Efficacy in Uveal Melanoma Is Linked to Tumor Immunity, CD28, and CCL8. International journal of molecular sciences 1 41155258
2025 CBX6 induces CD8+ T cell exhaustion and tumor development in esophageal squamous cell carcinoma through SMARCD1-mediated CCL8 secretion and lactate efflux. Cell biology and toxicology 1 41219497
2026 Targeting HSP90 suppresses STAT1/CCL8-driven inflammation and mitigates mitochondrial dysfunction to attenuate hypertension-induced atrial fibrillation. Life sciences 0 41720180
2026 P16+ Cells Drive Adverse Postischemic Cardiac Remodeling Through CCL8-Mediated Recruitment of Cytotoxic Lymphocytes. Circulation 0 41766526
2026 Histone demethylase JMJD1A protects mice from enteric bacterial infection by upregulating CCL8 expression to recruit macrophages and CD4+ T cells. PLoS pathogens 0 41779805
2026 CCL8-dependent recruitment of natural killer cells enhances the antitumor activity of neoadjuvant chemotherapy in gastric cancer. Cancer immunology, immunotherapy : CII 0 41843172
2026 Breast Cancer-Derived Extracellular Vesicle miR-425-5p (miR-425) Promotes Brain Metastasis via Activating Astrocytes Through the Novel miR-425-ZNF24-CCL8 Signaling Axis. International journal of molecular sciences 0 41977380
2026 Aging-Associated CCL8+ Senescent Macrophages Recruit CCR1+ Neutrophils to Promote NETs Formation and Impair Meningeal Lymphatic Drainage. Aging and disease 0 42065919
2025 Extracellular vesicle-derived miR-425-5p (miR-425) activates astrocytes in the brain to promote breast cancer brain metastasis via the novel miR-425-ZNF24-CCL8 signaling axis. bioRxiv : the preprint server for biology 0 40661472
2025 Role of CCL8 in cancer immunity and tumor progression: Implications for cancer treatment. Biochimica et biophysica acta. Reviews on cancer 0 41318072
2025 USP18 confers protection against allergic asthma by suppressing CCL8 production in alveolar type II epithelial cells. Respiratory research 0 41354823
2025 CCL8 suppresses ovarian cancer progression via M1 macrophage polarization and NF-κB-mediated apoptosis. Scientific reports 0 41408455

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