Affinage

CXCL17

C-X-C motif chemokine 17 · UniProt Q6UXB2

Length
119 aa
Mass
13.8 kDa
Annotated
2026-06-09
65 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CXCL17 is a mucosal chemoattractant chemokine that recruits monocytes, macrophages, myeloid-derived suppressor cells (MDSCs), and dendritic cells to epithelial and tumor microenvironments and shapes local immune tone (PMID:23115081, PMID:20955708, PMID:28389593). It is synthesized as a precursor that undergoes endoproteolytic maturation in gastric mucosa, and mature CXCL17 drives monocyte/macrophage chemotaxis through ERK1/2 and p38 signaling while inducing the proangiogenic factor VEGF-A and exerting anti-inflammatory effects on LPS-activated macrophages (PMID:23115081). Its principal signaling receptor is the orphan GPCR GPR25, which CXCL17 activates with ~100 nM potency to drive β-arrestin recruitment, TGF-α shedding, and chemotaxis through a two-step mechanism in which the GPR25 N-terminus orients the ligand so its essential C-terminal residues insert into the orthosteric pocket formed by GPR25 residues W95, R178, and R264 (PMID:40279398, PMID:42207165). Beyond its own receptor, CXCL17 acts as a glycosaminoglycan-dependent allosteric inhibitor of CXCR4 signaling and binds GAGs through C-terminal motifs, consistent with a non-classical chemokine fold (PMID:38502733, PMID:37942327). CXCL17 also possesses direct antimicrobial activity, killing bacteria by membrane disruption (PMID:22611239). The originally proposed receptor GPR35 ("CXCR8") does not transduce CXCL17 signaling: multiple independent laboratories found no activation across β-arrestin, inositol phosphate, calcium flux, endocytosis, TGF-α shedding, and chemotaxis assays, and GPR35 antagonists fail to block CXCL17-stimulated migration (PMID:29068046, PMID:29875152). In vivo, CXCL17 recruits MDSCs that promote tumor angiogenesis and metastasis via PDGF-BB while also restraining autoimmune and inflammatory pathology (PMID:22952881, PMID:30755260, PMID:30860634).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 2012 Medium

    Established that CXCL17 is not merely an immune signaling molecule but a direct effector with antimicrobial activity, defining a host-defense role at mucosal surfaces.

    Evidence In vitro antimicrobial assays against a bacterial panel with bacterial membrane disruption readout

    PMID:22611239

    Open questions at the time
    • Membrane-disruption mechanism not resolved at structural/residue level
    • No in vivo demonstration of antimicrobial protection
  2. 2012 Medium

    Defined CXCL17 as a maturation-processed chemoattractant for monocytes/macrophages acting through MAPK signaling, with angiogenic and anti-inflammatory consequences.

    Evidence Western blot for endoproteolysis, chemotaxis with ERK1/2/p38/JNK inhibitors, VEGF-A induction, and LPS-macrophage assays

    PMID:23115081

    Open questions at the time
    • Receptor mediating these effects not identified at the time
    • Protease responsible for endoproteolysis unknown
  3. 2014 Medium

    First proposed a receptor for CXCL17, naming GPR35 (CXCR8), to explain its chemoattractant activity and link it to lung macrophage recruitment.

    Evidence Calcium mobilization in GPR35-transfected Ba/F3 cells plus Cxcl17(-/-) mouse lung phenotype

    PMID:25411203

    Open questions at the time
    • Single calcium readout in one cell background
    • Subsequently contradicted by independent labs
  4. 2018 High

    Refuted the GPR35-CXCL17 pairing through multiple orthogonal signaling and chemotaxis assays, re-opening the question of the true CXCL17 receptor.

    Evidence AP-TGF-α shedding, β-arrestin, inositol phosphate, calcium, endocytosis, siRNA knockdown, and GPR35 antagonists (CID2745687, ML145) in THP-1 cells

    PMID:29068046 PMID:29875152

    Open questions at the time
    • Did not identify the actual receptor
    • Left mechanism of CXCL17 chemotaxis unexplained
  5. 2024 High

    Revealed a distinct mechanism by which CXCL17 modulates other chemokine axes, acting as a GAG-dependent allosteric inhibitor of CXCR4 rather than a direct agonist.

    Evidence BRET signaling/ligand-binding assays in intact cells, GAG-domain mutagenesis, GAG-binder mimicry (surfen, protamine), and neuropilin-1 interaction

    PMID:38502733

    Open questions at the time
    • Identity of the GAG-containing accessory protein not defined
    • Physiological relevance of CXCR4 inhibition not tested in vivo
  6. 2023 Medium

    Characterized CXCL17's biochemical behavior as a non-classical chemokine, showing GAG binding via C-terminal motifs and indirect modulation of CXCR1 signaling.

    Evidence Solid-phase GAG assays, bio-layer interferometry, structural modeling, and CXCR1 transfectant chemotaxis

    PMID:37942327

    Open questions at the time
    • No experimental structure to confirm non-canonical fold
    • Functional role of concentration-dependent dimerization unclear
  7. 2025 High

    Deorphanized GPR25 as a bona fide CXCL17 receptor and mapped the activation determinants, resolving the long-standing receptor question.

    Evidence AlphaFold 3 modeling, NanoBiT β-arrestin recruitment (EC50 ~100 nM) across 17 GPCRs, CXCL17 C-terminal truncation, and GPR25 W95/R178 alanine mutagenesis with TGF-α shedding/chemotaxis

    PMID:40279398

    Open questions at the time
    • Downstream G-protein coupling not fully dissected
    • No in vivo GPR25-CXCL17 genetic confirmation
  8. 2026 High

    Defined a two-step ligand-recognition mechanism in which the GPR25 N-terminus orients CXCL17 for C-terminus-driven activation, extending the deorphanization from an independent lab.

    Evidence GPR25 mutagenesis (W95/R178/R264), FPR1:GPR25 chimeras, CXCL17 N-terminal truncation, and L1.2 transfectant chemotaxis with computational modeling

    PMID:42207165

    Open questions at the time
    • High-resolution complex structure still lacking
    • Contribution of each step to signaling efficacy not quantified
  9. 2025 Medium

    Identified additional candidate receptors (MRGPRX2, MRGPRX1, MAS1) engaged through a C-terminus-independent mechanism distinct from GPR25, suggesting receptor multiplicity.

    Evidence NanoBiT β-arrestin assays and chemotaxis in HEK293T transfectants across 10 MRGPRs with CXCL17 C-terminal truncation

    PMID:41167449

    Open questions at the time
    • Micromolar potency raises physiological-relevance questions
    • No in vivo validation; awaits independent replication

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how CXCL17's multiple receptors (GPR25, MRGPRs), GAG-dependent allosteric activity, and direct antimicrobial function are integrated at native mucosal sites in vivo.
  • No structure of CXCL17 in complex with any receptor
  • Relative in vivo contributions of GPR25 vs MRGPR signaling unknown
  • GAG accessory protein required for CXCR4 inhibition unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 3 GO:0090729 toxin activity 1 GO:0098772 molecular function regulator activity 1
Localization
GO:0005576 extracellular region 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3
Partners
CXCR4GPR25NRP1

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 GPR35 (proposed as CXCR8) was identified as a receptor for CXCL17. Transfection of GPR35 into Ba/F3 cells rendered them responsive to CXCL17 as measured by calcium-mobilization assays. GPR35 expression is downregulated in lungs of Cxcl17(-/-) mice, which exhibit defects in macrophage recruitment to the lungs. Calcium mobilization assay in Ba/F3 transfectants; Cxcl17(-/-) mouse model with lung macrophage recruitment readout Journal of immunology Medium 25411203
2017 GPR35 does NOT mediate CXCL17-stimulated migration of THP-1 cells. In AP-TGF-α shedding assay using GPR35-overexpressing HEK293 cells, neither human nor mouse CXCL17 activated GPR35. GPR35 siRNA knockdown and the GPR35 antagonist CID2745687 blocked lodoxamide-induced migration inhibition but did not block CXCL17-stimulated migration of THP-1 cells, indicating CXCL17 signals through a receptor other than GPR35. AP-TGF-α shedding assay; siRNA knockdown of GPR35 in THP-1 cells; pharmacological antagonism with CID2745687; chemotaxis assay British journal of pharmacology High 29068046
2018 GPR35 failed to signal in response to CXCL17 in assays of β-arrestin recruitment, inositol phosphate production, calcium flux, and receptor endocytosis. In chemotaxis assays, GPR35 did not confer sensitivity to CXCL17. In THP-1 cells, CXCL17-stimulated migration was not blocked by the GPR35 antagonist ML145, indicating CXCL17 acts through an unidentified receptor distinct from GPR35. β-arrestin recruitment assay; inositol phosphate production assay; calcium flux assay; receptor endocytosis assay; TAXIScan real-time chemotaxis assay; pharmacological antagonism with ML145 Journal of immunology High 29875152
2012 CXCL17 has potent antimicrobial activity against a panel of pathogenic and opportunistic bacteria, and its mechanism of antimicrobial action involves peptide-mediated bacterial membrane disruption. In vitro antimicrobial assay against pathogenic bacteria panel; bacterial membrane disruption assay Journal of immunology Medium 22611239
2012 CXCL17 undergoes endoproteolysis during protein maturation in gastric mucosa. Mature CXCL17 acts as a chemoattractant for monocytes and macrophages, signaling through ERK1/2 and p38 but not JNK pathways. CXCL17 also induces production of proangiogenic factor VEGF-A from treated monocytes, and exhibits anti-inflammatory effects on LPS-activated macrophages. Western blotting for endoproteolysis; in vitro chemotaxis assay; signaling pathway inhibition (ERK1/2, p38, JNK); VEGF-A production assay; LPS-activated macrophage anti-inflammatory assay American journal of physiology. Endocrinology and metabolism Medium 23115081
2012 CXCL17 expressed by tumor cells recruits CD11b+Gr1(high)F4/80(-) myeloid-derived cells (approximately 90%, neutrophil-like morphology) as determined by chemotactic assays in vitro, and promotes tumor angiogenesis (CD31+ vessels) in vivo in immunodeficient mice. In vitro chemotaxis assay; in vivo xenograft tumor model with CXCL17-expressing NIH3T3 cells; flow cytometry; immunohistochemistry for CD31 PloS one Medium 22952881
2019 CXCL17 secreted by breast cancer cells increases accumulation of CD11b+Gr-1+ MDSCs in the lungs. These MDSCs express PDGF-BB, which mediates angiogenesis in the lung metastatic niche and facilitates cancer extravasation, colonization, and lung metastasis. In vitro chemotaxis assay; in vivo spontaneous metastasis mouse model; MDSC depletion; PDGF receptor inhibitor treatment; in vitro and in vivo models Breast cancer research : BCR Medium 30755260
2010 CXCL17 induces infiltration and accumulation of immature myeloid dendritic cells in the tumor epithelial layer, and this recruitment is followed by a cellular immune reaction in intraepithelial precursor lesions of pancreatic cancer (IPMN). The function was confirmed in syngeneic mouse models. Gene expression profiling; immunohistochemical analysis; syngeneic mouse model with functional readout (dendritic cell recruitment, immune response) Gastroenterology Medium 20955708
2018 CXCL17 is a direct target of miR-221-3p. CXCL17 inhibits expression of CCL24, CCL26, and periostin via the p38 MAPK pathway in bronchial epithelial cells. In a mouse model, overexpression of miR-221-3p suppressed CXCL17 expression and exacerbated airway eosinophilic inflammation. miR-221-3p target validation; siRNA/inhibitor experiments in BEAS-2B cells; p38 MAPK pathway inhibition assay; house dust mite mouse model with airway-specific miR-221-3p overexpression American journal of physiology. Lung cellular and molecular physiology Medium 29644894
2017 CXCL17 recruits CD11b+Gr-1+ MDSCs (but not Tregs) by direct chemotaxis in vitro. MDSCs then recruit Tregs through CCL5 and CCL4. Blockade of CCL5 or CCL4 abolished the anti-inflammatory effects of CXCL17 in an imiquimod-induced psoriasis-like skin inflammation model. In vitro chemotaxis assay for MDSCs and Tregs; in vivo injection of recombinant CXCL17; anti-CCL5/anti-CCL4 antibody blockade; flow cytometry; immunofluorescence Journal of immunology Medium 28389593
2018 CXCL17-/- mice showed reduced numbers of CXCR8+CD8+ TEM and TRM cells in the vaginal mucosa after intravaginal HSV-1 infection, associated with more virus replication and more latency in dorsal root ganglia. This indicates the CXCL17/CXCR8 pathway promotes mobilization of protective CD8+ TEM and TRM cells to mucosal tissues. Cxcl17(-/-) mouse model; intravaginal HSV-1 infection; flow cytometry for CD8+ T cell subsets; viral burden measurement; ganglia latency assay Journal of immunology Medium 29549178
2019 Cxcl17(-/-) mice have higher numbers of CD4+ and CD8+ T cells in spleen and lymph nodes, produce higher levels of proinflammatory cytokines upon activation, and develop exacerbated disease in an EAE model of T cell-dependent autoimmunity, with markedly reduced survival compared to wild-type littermates. Cxcl17(-/-) mouse model; T cell population analysis by flow cytometry; cytokine profiling; experimental autoimmune encephalomyelitis (EAE) model; survival analysis Journal of leukocyte biology Medium 30860634
2018 CXCL17 promotes cell metastasis and inhibits autophagy in hepatocellular carcinoma via the LKB1-AMPK pathway. Knockdown of CXCL17 activated AMPK and LKB1, enhanced nuclear translocation of LKB1, and stimulated autophagy markers (LC-3B, p62). Overexpression of CXCL17 suppressed these effects. CXCL17 siRNA knockdown and overexpression in HCC cells; Western blotting for AMPK, LKB1, LC-3B, p62; nuclear fractionation; invasion/migration assays Gene Low 30597237
2024 CXCL17 is an allosteric inhibitor of CXCR4. Using BRET-based assays, CXCL17 inhibited CXCR4-mediated signaling and ligand binding only in intact cells. This effect was mimicked by known glycosaminoglycan (GAG) binders (surfen, protamine sulfate), and disruption of putative GAG binding domains in CXCL17 prevented CXCR4 inhibition, indicating that CXCL17 requires GAG-containing accessory proteins to inhibit CXCR4. CXCL17 also interacted with neuropilin-1, a VEGFR2 co-receptor. BRET-based signaling and ligand binding assays; GAG domain mutagenesis in CXCL17; pharmacological mimicry with surfen and protamine sulfate; neuropilin-1 interaction assay Science signaling High 38502733
2023 CXCL17 binds efficaciously to glycosaminoglycans (GAGs) via key C-terminal motifs, as quantified by solid-phase assays and bio-layer interferometry. CXCL17 failed to adopt a classical chemokine fold by modeling. Recombinant CXCL17 dimerizes as a function of concentration. CXCL17 inhibited CXCR1-mediated chemotaxis of transfectants to CXCL8 in a dose-dependent manner but was inactive via CXCR1 directly. Solid-phase GAG binding assays; bio-layer interferometry; in silico structural modeling; chemotaxis assays with CXCR1 transfectants; recombinant protein production in mammalian and prokaryotic systems Frontiers in immunology Medium 37942327
2025 GPR25 was identified as a receptor for CXCL17 via AlphaFold 3 prediction and experimental validation. Recombinant CXCL17 activated human GPR25 in transfected HEK293T cells (EC50 ~100 nM) in a NanoBiT β-arrestin recruitment assay, but had no effect on 17 other GPCRs tested. Deletion of three conserved C-terminal residues from CXCL17 abolished activation. Alanine substitution of W95 or R178 in GPR25's predicted orthosteric binding pocket abolished response to CXCL17. Wild-type CXCL17 with wild-type GPR25 induced TGF-α shedding and chemotactic cell movement. AlphaFold 3 modeling; NanoBiT β-arrestin recruitment assay; C-terminal truncation mutagenesis of CXCL17; alanine mutagenesis of GPR25 binding pocket residues; TGF-α shedding assay; chemotaxis assay The FEBS journal High 40279398
2026 GPR25 mediates CXCL17-induced chemotaxis via a two-step mechanism: the GPR25 N-terminus orients CXCL17 for activation via its C-terminus. GPR25 residues W95, R178, and R264 are essential for chemotactic responsiveness. An N-terminally truncated CXCL17 (64-119) retains chemotactic activity via GPR25 but with reduced potency. A chimeric FPR1:GPR25 construct responded to CXCL17 with reduced potency, implicating the GPR25 N-terminus in recognition. Site-directed mutagenesis of GPR25; chimeric FPR1:GPR25 receptor constructs; N-terminal truncation of CXCL17; chemotaxis assay with L1.2 transfectants; computational modeling of CXCL17:GPR25 complex Basic & clinical pharmacology & toxicology High 42207165
2025 Human CXCL17 activates MRGPRX2, MRGPRX1, and MAS1 at micromolar concentrations in NanoBiT β-arrestin recruitment assays in transfected HEK293T cells, and induces chemotactic movement via these receptors. Removal of C-terminal residues from CXCL17 does not abolish MRGPR activation (in contrast to GPR25), indicating CXCL17 activates MRGPRs through a mechanism distinct from GPR25 activation. NanoBiT β-arrestin recruitment assay in HEK293T transfectants; C-terminal truncation mutagenesis of CXCL17; chemotaxis assay; panel of 10 human MRGPRs tested Archives of biochemistry and biophysics Medium 41167449
2024 Endothelial cell expression of CXCL17 is transcriptionally regulated by the YAP/TEAD1 complex activated by hypoxia-reoxygenation. CXCL17 recruits MDSCs (through binding to GPR35) during liver ischemia-reperfusion injury, and these MDSCs attenuate injury by inhibiting M1 macrophage polarization via upregulation of STAT3 signaling. Bulk RNA-sequencing; scRNA-seq; αGr-1 antibody depletion; adoptive transfer of MDSCs; in vivo mouse IRI model; hepatic endothelial cell hypoxia-reoxygenation stimulation; ChIP/transcription factor analysis implied Hepatology Medium 38407233
2020 CXCL17 reduces type I collagen expression in skin fibroblasts by inducing MMP1 and miR-29 expression, indicating post-transcriptional regulation of collagen via these effectors. Local injection of CXCL17 attenuated bleomycin-induced skin fibrosis in mice. Western blotting; RT-PCR for collagen, MMP1, miR-29; bleomycin mouse model with CXCL17 injection; ELISA for serum CXCL17 Journal of dermatological science Medium 33055012
2021 In intestinal epithelial cells (Caco-2), mycotoxins trigger ROS-dependent CXCL17 production via p38 and JNK pathways. CXCL17 then mediates immunoprotective responses (reduced inflammation and apoptosis) through the PI3K/AKT/mTOR pathway. Caco-2 cell model; ROS measurement; signaling pathway inhibitors (p38, JNK, PI3K/AKT/mTOR); apoptosis and inflammation assays Biochemical pharmacology Low 33932472
2019 CXCL17 increases migration of THP-1 mononuclear macrophages by activating the Src/FAK signaling pathway, as demonstrated by Western blotting. M2 macrophages polarized in conditioned media promoted proliferation of lung adenocarcinoma cells. Transwell invasion assay; Western blotting for Src and FAK phosphorylation; conditioned medium from M1/M2 macrophages; CCK-8 proliferation assay Cellular oncology Low 31832986
2023 Recombinant CXCL17 treatment alleviates hyperoxia-induced lung injury in neonatal mice by activating the AKT pathway, reducing apoptosis, oxidative stress, and inflammation, as validated in both a mouse model and primary murine alveolar epithelial type II cells. Hyperoxia mouse model; recombinant CXCL17 treatment; Western blotting for AKT pathway; TUNEL staining for apoptosis; ELISA for inflammatory factors; DHE staining for ROS Molecular biotechnology Low 37710083
2025 CXCL17 promotes cardiac fibroblast proliferation by activating AKT signaling and upregulating bFGF in a positive feedback loop. Both CXCL17 and bFGF activate AKT signaling synergistically. In vivo, CXCL17 increased cardiac fibrosis in an isoprenaline-induced mouse model, reversible by a CXCL17-blocking antibody. In vitro fibroblast proliferation assay; Western blotting for AKT signaling; bFGF measurement; isoprenaline mouse model; CXCL17-blocking antibody treatment Cardiovascular journal of Africa Low 40778660

Source papers

Stage 0 corpus · 65 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 CXCL17 and ICAM2 are associated with a potential anti-tumor immune response in early intraepithelial stages of human pancreatic carcinogenesis. Gastroenterology 146 20955708
2014 Cutting edge: GPR35/CXCR8 is the receptor of the mucosal chemokine CXCL17. Journal of immunology (Baltimore, Md. : 1950) 125 25411203
2019 CXCL17-derived CD11b+Gr-1+ myeloid-derived suppressor cells contribute to lung metastasis of breast cancer through platelet-derived growth factor-BB. Breast cancer research : BCR 84 30755260
2012 CXCL17 is a mucosal chemokine elevated in idiopathic pulmonary fibrosis that exhibits broad antimicrobial activity. Journal of immunology (Baltimore, Md. : 1950) 80 22611239
2012 CXCL17 expression by tumor cells recruits CD11b+Gr1 high F4/80- cells and promotes tumor progression. PloS one 78 22952881
2012 CXCL17, an orphan chemokine, acts as a novel angiogenic and anti-inflammatory factor. American journal of physiology. Endocrinology and metabolism 74 23115081
2006 VCC-1, a novel chemokine, promotes tumor growth. Biochemical and biophysical research communications 68 16989774
2018 Decreased epithelial and sputum miR-221-3p associates with airway eosinophilic inflammation and CXCL17 expression in asthma. American journal of physiology. Lung cellular and molecular physiology 62 29644894
2020 The protective and pathogenic roles of CXCL17 in human health and disease: Potential in respiratory medicine. Cytokine & growth factor reviews 61 32345516
2017 CXCL17 Attenuates Imiquimod-Induced Psoriasis-like Skin Inflammation by Recruiting Myeloid-Derived Suppressor Cells and Regulatory T Cells. Journal of immunology (Baltimore, Md. : 1950) 58 28389593
2017 GPR35 mediates lodoxamide-induced migration inhibitory response but not CXCL17-induced migration stimulatory response in THP-1 cells; is GPR35 a receptor for CXCL17? British journal of pharmacology 56 29068046
2017 The role and clinical significance of the CXCL17-CXCR8 (GPR35) axis in breast cancer. Biochemical and biophysical research communications 53 28943434
2018 CXCL17 Chemokine-Dependent Mobilization of CXCR8+CD8+ Effector Memory and Tissue-Resident Memory T Cells in the Vaginal Mucosa Is Associated with Protection against Genital Herpes. Journal of immunology (Baltimore, Md. : 1950) 50 29549178
2016 Ectopic expression of the chemokine CXCL17 in colon cancer cells. British journal of cancer 46 26889977
2023 Tumor-associated macrophages confer colorectal cancer 5-fluorouracil resistance by promoting MRP1 membrane translocation via an intercellular CXCL17/CXCL22-CCR4-ATF6-GRP78 axis. Cell death & disease 43 37658050
2018 Evidence for the Existence of a CXCL17 Receptor Distinct from GPR35. Journal of immunology (Baltimore, Md. : 1950) 43 29875152
2021 Exosomal DLX6-AS1 from hepatocellular carcinoma cells induces M2 macrophage polarization to promote migration and invasion in hepatocellular carcinoma through microRNA-15a-5p/CXCL17 axis. Journal of experimental & clinical cancer research : CR 41 34039401
2020 Mucosal chemokine CXCL17: What is known and not known. Scandinavian journal of immunology 39 32869346
2016 Characterization of VCC-1, a Novel Ambler Class A Carbapenemase from Vibrio cholerae Isolated from Imported Retail Shrimp Sold in Canada. Antimicrobial agents and chemotherapy 38 26824956
2018 CXCL17 promotes cell metastasis and inhibits autophagy via the LKB1-AMPK pathway in hepatocellular carcinoma. Gene 37 30597237
2019 Tumor cell expression of B7-H4 correlates with higher frequencies of tumor-infiltrating APCs and higher CXCL17 expression in human epithelial ovarian cancer. Oncoimmunology 35 31741762
2009 Overexpression of VCC-1 gene in human hepatocellular carcinoma cells promotes cell proliferation and invasion. Acta biochimica et biophysica Sinica 32 19657564
2018 Kynurenic acid and zaprinast diminished CXCL17-evoked pain-related behaviour and enhanced morphine analgesia in a mouse neuropathic pain model. Pharmacological reports : PR 27 30550994
2024 Endothelial YAP/TEAD1-CXCL17 signaling recruits myeloid-derived suppressor cells against liver ischemia-reperfusion injury. Hepatology (Baltimore, Md.) 23 38407233
2021 MiR-325-3p mediate the CXCL17/CXCR8 axis to regulate angiogenesis in hepatocellular carcinoma. Cytokine 23 33515898
2019 Cxcl17-/- mice develop exacerbated disease in a T cell-dependent autoimmune model. Journal of leukocyte biology 23 30860634
2019 MiR-4513 mediates the proliferation and apoptosis of oral squamous cell carcinoma cells via targeting CXCL17. European review for medical and pharmacological sciences 22 31115009
2019 Mechanism of lung adenocarcinoma spine metastasis induced by CXCL17. Cellular oncology (Dordrecht, Netherlands) 20 31832986
2022 Involvement of CXCL17 and GPR35 in Gastric Cancer Initiation and Progression. International journal of molecular sciences 19 36614059
2024 CXCL17 is an allosteric inhibitor of CXCR4 through a mechanism of action involving glycosaminoglycans. Science signaling 15 38502733
2023 What defines a chemokine? - The curious case of CXCL17. Cytokine 15 37210967
2024 Characterization of prostate macrophage heterogeneity, foam cell markers, and CXCL17 upregulation in a mouse model of steroid hormone imbalance. Scientific reports 13 39251671
2023 CXCL17 binds efficaciously to glycosaminoglycans with the potential to modulate chemokine signaling. Frontiers in immunology 13 37942327
2022 The cryptic role of CXCL17/CXCR8 axis in the pathogenesis of cancers: a review of the latest evidence. Journal of cell communication and signaling 13 36352331
2023 CXCL17 Attenuates Diesel Exhaust Emissions Exposure-Induced Lung Damage by Regulating Macrophage Function. Toxics 12 37624152
2012 VCC-1 over-expression inhibits cisplatin-induced apoptosis in HepG2 cells. Biochemical and biophysical research communications 12 22425983
2024 Overexpression of CXCL17 increases migration and invasion of A549 lung adenocarcinoma cells. Frontiers in pharmacology 11 38384293
2020 CXCL17-mediated downregulation of type I collagen via MMP1 and miR-29 in skin fibroblasts possibly contributes to the fibrosis in systemic sclerosis. Journal of dermatological science 11 33055012
2023 Activation of the IL-17 signalling pathway by the CXCL17-GPR35 axis affects drug resistance and colorectal cancer tumorigenesis. American journal of cancer research 10 37293165
2022 Expression and clinical significance of CXCL17 and GPR35 in endometrial carcinoma. Anti-cancer drugs 9 35276691
2022 A comprehensive review of chemokine CXC17 (VCC1) in cancer, infection, and inflammation. Cell biology international 9 35811438
2022 THUMPD3-AS1 Is Correlated with Gastric Cancer and Regulates Cell Function through miR-1252-3p and CXCL17. Critical reviews in eukaryotic gene expression 9 36017917
2021 Intestinal guard: Human CXCL17 modulates protective response against mycotoxins and CXCL17-mimetic peptides development. Biochemical pharmacology 9 33932472
2025 Identification of orphan GPR25 as a receptor for the chemokine CXCL17. The FEBS journal 7 40279398
2019 Association Between Unstable Angina and CXCL17: a New Potential Biomarker. Open medicine (Warsaw, Poland) 6 31934638
2024 Analysis of the mucosal chemokines CCL28, CXCL14, and CXCL17 in dry eye disease: An in vitro and clinical investigation. Experimental eye research 5 38453037
2021 CXCL17 Is Dispensable during Hypervirulent Mycobacterium tuberculosis HN878 Infection in Mice. ImmunoHorizons 5 34561226
2019 Molecular Basis for the Potent Inhibition of the Emerging Carbapenemase VCC-1 by Avibactam. Antimicrobial agents and chemotherapy 5 30782990
2025 Deficiency of antioxidant enzyme PRDX6 and mucosal chemokine CXCL17: unraveling the factors behind oxidative stress and mucosal homeostasis disruption in dry eye disease. Biochimica et biophysica acta. Molecular basis of disease 3 40441367
2025 Human CXCL17 binds and activates fish GPR25 orthologs. Biochimie 3 40972788
2026 Identification and functional characterization of two CXCL17 paralogs from zebrafish. The Biochemical journal 2 41521655
2025 CXCL17 activates three MAS-related G protein-coupled receptors independently of its conserved C-terminal fragment. Archives of biochemistry and biophysics 2 41167449
2023 Recombinant CXCL17 Treatment Alleviates Hyperoxia-Induced Lung Apoptosis and Inflammation In Vivo and Vitro by Activating the AKT Pathway: A Possible Therapeutic Approach for Bronchopulmonary Dysplasia. Molecular biotechnology 2 37710083
2017 Enhancement of ERK phosphorylation and photic responses in Vc/C1 neurons of a migraine model. Neuroscience letters 2 28323089
2026 Identification and functional characterization of CXCL17 orthologs in amphibians. Archives of biochemistry and biophysics 1 41861938
2023 Plasmid-encoded VCC-1 β-lactamase in a clinical isolate of Aeromonas caviae. Antimicrobial agents and chemotherapy 1 37889006
2023 Effect of CXCL17 on Subcutaneous Preadipocytes Proliferation in Goats. Animals : an open access journal from MDPI 1 37889664
2026 Clinical significance of CXCL17 in cervical cancer. Medicine 0 41496085
2026 SNRPC promotes chemoresistance in Wilms tumor via the NF-κB-CXCL17 axis regulating M2-Type TAMs infiltration and targeted nanotherapy research. Journal of experimental & clinical cancer research : CR 0 41761364
2026 Single-cell transcriptome analysis reveals DNMT1+ epithelial cells promote lymphatic metastasis via CXCL17-mediated TAM infiltration. Journal of translational medicine 0 41845371
2026 Ancestral origin of the CXCL17-GPR25 system traced to the lobe-finned fish Latimeria chalumnae. Biochimie 0 41887359
2026 Evidence for a Two-Step Model for Activation of GPR25 by the Chemoattractant CXCL17. Basic & clinical pharmacology & toxicology 0 42207165
2025 CXCL17 promotes cardiac fibroblasts proliferation and fibrosis by up-regulating bFGF in a positive loop. Cardiovascular journal of Africa 0 40778660
2024 PROSTATE CELL HETEROGENEITY AND CXCL17 UPREGULATION IN MOUSE STEROID HORMONE IMBALANCE. bioRxiv : the preprint server for biology 0 38712029
2024 Loss of CCL28 and CXCL17 Expression and Increase in CCR1 Expression May Be Related to Malignant Transformation of LGBLEL into Lymphoma. Current issues in molecular biology 0 39451532

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