Affinage

CXCL11

C-X-C motif chemokine 11 · UniProt O14625

Length
94 aa
Mass
10.4 kDa
Annotated
2026-04-28
100 papers in source corpus 35 papers cited in narrative 35 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CXCL11 is an interferon-inducible, non-ELR CXC chemokine that functions as the highest-affinity ligand for CXCR3, driving chemotaxis of activated T cells, macrophages, and keratinocytes while also acting as a natural antagonist at CCR3 and CCR5 and serving as a scavenged ligand for the decoy receptor CACKR3/CXCR7 (PMID:9625760, PMID:11110785, PMID:15178708, PMID:16940167). Signaling through CXCR3 activates Gαi-dependent calcium flux, PLC-β3/μ-calpain-mediated focal adhesion disassembly in keratinocytes, ERK1/2-driven proliferation and stemness programs, and an mTOR/STAT3/STAT6-dependent immunotolerizing pathway that polarizes T cells toward Tr1/Th2 fates — distinguishing CXCL11 from the Th1-promoting ligand CXCL10 despite sharing the same receptor (PMID:15713646, PMID:24713654, PMID:30771435). CXCL11 activity is tightly regulated post-translationally: DPP IV N-terminal cleavage abolishes agonism, MMP-mediated truncation converts it to a CXCR3 antagonist, citrullination by PAD impairs signaling, and C-terminal helix residues mediating glycosaminoglycan binding are required for in vivo gradient formation and leukocyte recruitment (PMID:12101279, PMID:18411283, PMID:18645041, PMID:20363748). Transcriptional induction requires TYK2 kinase activity, a non-canonical unphosphorylated STAT3 scaffold that recruits NF-κB p65 and IRF1 to the promoter, STAT2/IRF9 in response to IFNα, and PRMT5-dependent symmetric dimethylation of p65 Arg174 (PMID:9890942, PMID:17202361, PMID:28472186, PMID:26901772).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1998 High

    Establishing that CXCL11 is a CXCR3-selective chemokine with the highest receptor affinity among its family members resolved the identity and primary receptor for this IFN-inducible chemokine and defined its cellular target as activated T cells.

    Evidence Receptor binding assays, calcium flux, and chemotaxis in IL-2-activated T cells and CXCR3 transfectants

    PMID:9625760

    Open questions at the time
    • Downstream intracellular signaling cascades not yet mapped
    • In vivo relevance of CXCR3 selectivity untested
  2. 1999 High

    Demonstrating that CXCL11 induction requires catalytically active TYK2 beyond the canonical ISGF3 pathway established that CXCL11 transcription depends on a specialized IFN signaling branch distinct from typical ISGs.

    Evidence TYK2-deficient cell complementation with kinase-dead mutants and promoter-reporter assays

    PMID:9890942

    Open questions at the time
    • Downstream TYK2 substrates specific to CXCL11 induction not identified
    • Whether TYK2 requirement extends to IFN-γ vs. IFN-β not resolved
  3. 2000 High

    Revealing that CXCL11 acts as a natural antagonist of CCR3 expanded its functional repertoire beyond CXCR3 agonism to include counter-regulation of eosinophil chemotaxis, providing a mechanism for cross-talk between Th1 and Th2 chemokine systems.

    Evidence Competitive binding, calcium flux, and chemotaxis assays with CCR3 transfectants and human eosinophils

    PMID:11110785

    Open questions at the time
    • Structural basis of CCR3 antagonism vs. CXCR3 agonism unknown
    • In vivo relevance of CCR3 antagonism not tested
  4. 2002 High

    Identifying DPP IV-mediated N-terminal cleavage as an inactivation mechanism established the first post-translational regulatory switch for CXCL11 and showed the truncated product acts as a desensitizing agent.

    Evidence Mass spectrometry of cleavage product, calcium flux and chemotaxis assays with T cells

    PMID:12101279

    Open questions at the time
    • Relative contribution of DPP IV cleavage vs. other proteases in vivo unclear
    • Whether truncated CXCL11(3-73) has physiological antagonist function in tissues untested
  5. 2003 High

    Showing that CXCL11 activates CXCR3-B to mediate angiostatic effects on endothelial cells revealed that receptor splice variant usage determines whether CXCL11 promotes migration or inhibits proliferation/induces apoptosis.

    Evidence HMEC-1 transfection with CXCR3-A or CXCR3-B, radioligand binding, DNA synthesis, apoptosis assays

    PMID:12782716

    Open questions at the time
    • Relative expression levels of CXCR3-A vs. CXCR3-B across tissues not systematically mapped
    • Signaling pathways downstream of CXCR3-B not fully delineated
  6. 2004 High

    Mapping the intracellular domains of CXCR3 required for CXCL11 vs. CXCL10/CXCL9 responses demonstrated biased agonism at the receptor level — CXCL11 uniquely requires the third intracellular loop for internalization while other ligands require the C-terminus and β-arrestin1, and CXCL11 also antagonizes CCR5 via specific surface residues.

    Evidence CXCR3 deletion/point mutants with internalization, chemotaxis, and calcium assays; CCR5 competitive binding and structure-activity analysis

    PMID:15150261 PMID:15178708

    Open questions at the time
    • Whether biased signaling translates to distinct gene expression programs in T cells unknown
    • Crystal structure of CXCL11-CXCR3 complex unavailable
  7. 2004 High

    Solving the NMR structure of CXCL11 revealed a monomeric chemokine with a beta-bulge preventing dimerization, providing a structural explanation for its distinct receptor binding properties.

    Evidence Solution NMR structure determination

    PMID:15273303

    Open questions at the time
    • No CXCL11-receptor complex structure
    • Functional significance of obligate monomerism vs. other CXCR3 ligands unexplored
  8. 2005 High

    Multiple 2005 studies established diverse biological outputs: CXCL11 promotes keratinocyte wound healing via PLC-β3/μ-calpain/FAK cleavage, drives CD8+ T cell-dependent antitumor immunity in vivo, inhibits osteoclastogenesis downstream of IFN-β, and is required for wound maturation in vivo.

    Evidence RNAi distinguishing calpain isoforms in keratinocytes; EL4 tumor model with CD8 depletion; monocyte osteoclast differentiation assays; antisense transgenic wound model

    PMID:15713646 PMID:16000952 PMID:16081539 PMID:18669615

    Open questions at the time
    • Whether μ-calpain pathway operates in non-keratinocyte CXCR3+ cells unknown
    • Relative contribution of CXCL11 vs. CXCL9/10 to CD8 T cell tumor recruitment not dissected
  9. 2006 High

    Identifying CXCR7 as a high-affinity alternate receptor for CXCL11 that does not couple to G-proteins but promotes cell survival and adhesion revealed a second receptor system operating as a ligand sink.

    Evidence Radioligand binding, calcium and migration assays (negative), adhesion and tumor growth assays in vivo

    PMID:16940167

    Open questions at the time
    • Signaling pathways downstream of CXCR7 upon CXCL11 binding not identified
    • Relative contribution of CXCR7 scavenging to CXCL11 gradient shaping in vivo unclear
  10. 2007 High

    Demonstrating that STAT3 (independent of Y705 phosphorylation) scaffolds NF-κB p65 and IRF1 onto the CXCL11 promoter while its absence permits repressor binding resolved the non-canonical transcription factor requirement for CXCL11 induction.

    Evidence STAT3-deficient cells with WT/Y705F reconstitution, ChIP at CXCL11 promoter, promoter-reporter assays

    PMID:17202361

    Open questions at the time
    • Direct protein-protein interaction between unphosphorylated STAT3, p65, and IRF1 not biochemically reconstituted
    • Whether this non-canonical STAT3 mechanism operates in all CXCL11-producing cell types untested
  11. 2008 High

    Characterizing MMP-mediated proteolytic processing and PAD-mediated citrullination as two additional post-translational regulatory mechanisms showed that CXCL11 can be converted from agonist to antagonist (by MMPs) or functionally attenuated (by citrullination), with C-terminal truncation ablating both receptor and GAG binding.

    Evidence MALDI-TOF MS of MMP cleavage products with chemotaxis/heparin binding; PAD citrullination with MS and functional assays

    PMID:18411283 PMID:18645041

    Open questions at the time
    • In vivo prevalence of citrullinated vs. MMP-truncated CXCL11 forms unknown
    • Which MMP family members are most relevant in specific tissue contexts not established
  12. 2010 High

    Mapping the GAG-binding epitope to C-terminal helix residues K57-K58-R62 and K17 and showing that GAG-binding mutants fail in vivo despite normal in vitro chemotaxis established that heparan sulfate immobilization is essential for CXCL11 gradient function in tissues; separately, CXCR7 was confirmed as a constitutively cycling scavenger that internalizes and degrades CXCL11.

    Evidence Alanine-scanning mutagenesis with in vitro/in vivo migration assays; live-cell imaging of CXCR7 cycling and ligand degradation in mammalian cells and zebrafish

    PMID:20161793 PMID:20363748

    Open questions at the time
    • Tissue-specific GAG composition effects on CXCL11 gradient formation unknown
    • Relative quantitative contribution of CXCR7 vs. DPP IV/MMPs to CXCL11 clearance in vivo not determined
  13. 2014 High

    Demonstrating that CXCL11 and CXCL10 activate distinct signaling cascades through the same receptor — CXCL11 driving mTOR/STAT3/STAT6-dependent Tr1/Th2 tolerance vs. CXCL10 driving STAT1/4/5-dependent Th1 immunity — resolved a long-standing puzzle of how three ligands sharing one receptor produce opposing immunological outcomes.

    Evidence T cell polarization, phospho-STAT blots, mTOR inhibitors, CXCL11-Ig fusion therapeutic in EAE model

    PMID:24713654

    Open questions at the time
    • Structural basis for biased agonism at CXCR3 not determined
    • Whether tolerance-inducing pathway operates in all T cell subsets or disease contexts unknown
  14. 2016 High

    Identifying PRMT5-mediated Arg174 dimethylation of NF-κB p65 as required for p65 association with the CXCL11 promoter added an epigenetic regulatory layer to CXCL11 transcription; separately, systematic ACKR3 mutagenesis revealed a CXCL11 binding mode distinct from CXCL12, with scavenging decoupled from arrestin recruitment.

    Evidence PRMT5 RNAi, p65 R174 mutant reconstitution, ChIP/Re-ChIP; 30 ACKR3 substitution mutants with binding, arrestin, and scavenging assays

    PMID:26901772 PMID:27875312

    Open questions at the time
    • Whether PRMT5-p65 methylation is a general NF-κB target gene mechanism or CXCL11-selective unclear
    • ACKR3-mediated signaling events independent of G-proteins and arrestins not identified
  15. 2017 Medium

    Establishing STAT2/IRF9 (but not STAT1) as required for IFNα-induced CXCL11 expression in keratinocytes identified a cell-type-specific transcriptional input distinct from the STAT3/IRF1 axis described in other contexts.

    Evidence STAT2 siRNA in keratinocytes, 102-cytokine multiplex screen, IRF9/STAT1/STAT6 knockdowns

    PMID:28472186

    Open questions at the time
    • Whether STAT2/IRF9 and STAT3/IRF1 pathways converge or operate in distinct cell types not resolved
    • Promoter occupancy by STAT2/IRF9 not demonstrated by ChIP in this study
  16. 2019 Medium

    Two studies extended CXCL11 biology to tumor microenvironment signaling: docetaxel-induced HMGB1 stimulates CXCL11 via NF-κB to recruit CD8+ T cells, while autocrine CXCL11/CXCR3/ERK1/2 signaling maintains stemness in hepatocellular carcinoma tumor-initiating cells.

    Evidence HMGB1-NF-κB-CXCL11 pathway analysis with ROS inhibition and in vivo CAR T recruitment; CXCR3 blocking and ERK inhibition in HCC sphere assays

    PMID:30744691 PMID:30771435

    Open questions at the time
    • Whether CXCL11-driven stemness operates in tumor types beyond HCC untested
    • Relative importance of CXCL11 vs. CXCL9/10 in docetaxel-induced immune recruitment not quantified
  17. 2021 Medium

    Showing that RBM15 stabilizes CXCL11 mRNA via m6A modification to promote macrophage infiltration and M2 polarization in ccRCC introduced epitranscriptomic regulation as a mechanism controlling CXCL11 abundance.

    Evidence RBM15 knockdown/overexpression, m6A assays, mRNA stability measurements, macrophage co-culture, xenograft models

    PMID:35381326

    Open questions at the time
    • Specific m6A sites on CXCL11 mRNA not mapped
    • Whether m6A-dependent regulation operates outside ccRCC unclear
    • Reader proteins mediating m6A-dependent CXCL11 stability not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of biased agonism at CXCR3 (no CXCL11-CXCR3 complex structure exists), the in vivo quantitative hierarchy among the multiple post-translational regulatory mechanisms (DPP IV, MMPs, PAD, CXCR7 scavenging), and whether CXCL11's immunotolerizing signaling can be therapeutically harnessed independently of its chemotactic function.
  • No atomic-resolution CXCL11-CXCR3 complex structure
  • Quantitative in vivo contribution of each proteolytic/PTM pathway to CXCL11 regulation not established
  • Therapeutic separation of tolerogenic vs. chemotactic functions not achieved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 7 GO:0098772 molecular function regulator activity 2
Localization
GO:0005576 extracellular region 4
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-168256 Immune System 5
Partners
ACKR3CCR3CCR5CXCR3DPP4

Evidence

Reading pass · 35 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 CXCL11 (I-TAC) was identified as a novel non-ELR CXC chemokine that binds selectively to CXCR3 with higher affinity than CXCL9 or CXCL10, induces transient intracellular calcium mobilization and chemotactic migration in IL-2-activated T cells and CXCR3-transfected cell lines, but not in neutrophils or monocytes. Receptor binding assays, calcium flux assays, chemotaxis assays in activated T cells and CXCR3 transfectants The Journal of experimental medicine High 9625760
2003 CXCL11 binds and activates CXCR3-B, an alternatively spliced variant of CXCR3, which mediates angiostatic (anti-proliferative/pro-apoptotic) effects on endothelial cells, distinct from the pro-survival signaling of CXCR3-A. HMEC-1 transfection with CXCR3-A or CXCR3-B constructs, radioligand binding, DNA synthesis assays, apoptosis assays, signal transduction analysis The Journal of experimental medicine High 12782716
2000 CXCL11, CXCL9, and CXCL10 (CXCR3 agonists) act as natural antagonists for CCR3, competing for eotaxin binding to CCR3-bearing cells and inhibiting CCR3-mediated migration and Ca2+ responses without inducing CCR3 internalization; CXCL11 was the most efficacious antagonist. Competitive binding assays, calcium flux assays, chemotaxis assays with CCR3 transfectants and human eosinophils; hybrid chemokine construction The Journal of biological chemistry High 11110785
2006 CXCL11 (I-TAC) binds with high affinity to CXCR7 (RDC1), an alternate receptor that does not couple to G-proteins or induce calcium mobilization or cell migration, but instead confers cell survival and adhesion advantages; CXCR7 expression promotes in vivo tumor growth. Radioligand binding, calcium mobilization assays, cell migration assays, adhesion assays, small molecule antagonist studies, in vivo tumor models The Journal of experimental medicine High 16940167
2010 CXCR7 functions as a scavenger receptor for CXCL11 and CXCL12, mediating constitutive ligand internalization and targeting chemokines for lysosomal degradation without G-protein coupling; CXCR7 continuously cycles between plasma membrane and intracellular compartments in both mammalian cells and zebrafish. Ligand internalization assays, degradation assays, live-cell imaging/receptor cycling assays in mammalian cells and zebrafish; active CXCL12 sequestration demonstrated in mouse heart valves and human umbilical vein endothelium PloS one High 20161793
2004 CXCL11 uses distinct intracellular domains of CXCR3 for internalization: the third intracellular loop is predominantly required for CXCL11-induced CXCR3 internalization, whereas CXCL9 and CXCL10 require the carboxyl-terminal domain and beta-arrestin1. All three ligands require the carboxyl terminus and DRY sequence for chemotaxis and calcium mobilization. CXCR3 deletion/point mutants expressed in cells, internalization assays, chemotaxis assays, calcium mobilization assays, beta-arrestin co-immunoprecipitation The Journal of biological chemistry High 15150261
2002 Dipeptidyl peptidase IV (DPP IV/CD26) expressed on T cells cleaves CXCL11 at its N-terminus (removing two residues to generate CXCL11(3-73)), reducing CXCR3 binding ~8-fold, completely abolishing calcium flux and chemotaxis, but retaining partial CXCR3 downregulation activity so the truncated form desensitizes T cells to intact CXCL11. DPP IV inhibitor experiments, mass spectrometry characterization of cleavage product, calcium flux assays, chemotaxis assays, CXCR3 binding assays with T cells and transfectants Journal of leukocyte biology High 12101279
2008 Matrix metalloproteinases MMP-8, MMP-12, and MMP-9 cleave CXCL11 at both amino and carboxyl termini, generating CXCL11-(5-73), -(5-63), and -(5-58) forms. N-terminal truncation converts CXCL11 from a CXCR3 agonist to an antagonist with enhanced heparin affinity (CXCL11-(5-73)); further C-terminal truncation to position 58 abolishes both antagonist activity and heparin binding. MALDI-TOF mass spectrometry identification of cleavage products, calcium mobilization assays, chemotaxis assays with CXCR3 transfectants and human T lymphocytes, heparin binding assays The Journal of biological chemistry High 18411283
2008 Peptidylarginine deiminase (PAD) citrullinates CXCL11 by converting arginine to citrulline, impairing CXCR3 signaling and T-cell activation without altering receptor binding, and reducing heparin binding properties of CXCL11. In vitro citrullination with rabbit PAD and human PAD2, mass spectrometry, calcium mobilization assays, chemotaxis assays, heparin binding assays, CXCR3 binding assays Blood High 18645041
2004 CXCL11 acts as a natural antagonist for CCR5: it inhibits MIP-1α/CCL3 binding to CCR5-transfected cells and monocytes, and blocks CCR5-mediated cell migration, calcium release, and actin polymerization; structural analysis implicates residues K17, K49, and Q51 of CXCL11 in CCR5 binding. Competitive binding assays, chemotaxis assays, calcium flux assays, actin polymerization assays with CCR5 transfectants and primary monocytes; structure-activity analysis Journal of leukocyte biology High 15178708
2004 NMR solution structure of CXCL11 reveals the canonical chemokine fold with greater conformational flexibility than related chemokines; CXCL11 contains a beta-bulge in beta-strand 1 that distorts the dimerization interface and prevents dimer formation at millimolar concentrations, unlike CXCL10 and IL-8. Solution NMR structure determination Protein science High 15273303
2005 CXCL11 (IP-9) promotes keratinocyte motility via CXCR3 signaling through a pathway requiring phospholipase C-β3-dependent intracellular calcium flux and selective activation of mu-calpain (calpain 1), leading to cleavage of focal adhesion kinase and disassembly of vinculin aggregates; this is distinct from EGF-induced motility which requires M-calpain (calpain 2). In vitro wound healing assay, pharmacological inhibitors of PLC-β3 and calcium chelation, RNAi-mediated depletion of calpain 1 vs. calpain 2, focal adhesion kinase cleavage assays, vinculin immunofluorescence Molecular and cellular biology High 15713646
1999 IFN-beta induction of CXCL11 (beta-R1/I-TAC) requires catalytically active TYK2 kinase; cells expressing kinase-deficient TYK2 mutants fail to induce CXCL11 despite normal expression of other IFN-stimulated genes, indicating CXCL11 induction depends on an accessory TYK2-dependent signaling pathway beyond the canonical ISGF3/ISRE pathway. TYK2-deficient U1 cell complementation with wild-type or kinase-dead TYK2 mutants, promoter-reporter transfection assays, comparison of CXCL11 vs. other ISG induction The Journal of biological chemistry High 9890942
2007 CXCL11 gene induction by IFN requires STAT3 in a non-canonical manner: STAT3 is required but Y705 phosphorylation is not needed; STAT3 recruits transcriptional activators NF-κB p65 and IRF1 to the CXCL11 promoter, while its absence leads to binding of repressors p50 and IRF2. STAT3-deficient cell lines, wild-type and Y705F STAT3 reconstitution, chromatin immunoprecipitation assays of CXCL11 promoter, promoter-reporter assays Journal of immunology High 17202361
2016 PRMT5-mediated symmetric dimethylation of NF-κB p65 at Arg174 is required for TNF-α plus IFN-γ-induced CXCL11 gene expression in endothelial cells; p65 Arg174Ala or Arg174Lys mutants fail to associate with the CXCL11 promoter, and PRMT5 knockdown reduces CXCL11 mRNA and protein. PRMT5 RNAi, p65 Arg174 mutant reconstitution, mass spectrometric identification of methylation site, ChIP and Re-ChIP assays at CXCL11 promoter PloS one High 26901772
2010 GAG-binding epitope of CXCL11 maps primarily to the C-terminal helix residues K57-K58-Q-A-R62 plus K17; mutation of these residues impairs heparin binding in vitro and abolishes in vivo cell migration despite retained receptor binding and near-normal in vitro chemotaxis, establishing a requirement for GAG interactions for CXCL11 in vivo function. CXCL11 also exhibits two affinity states for both heparin and CXCR3, likely related to its conformational flexibility. Alanine-scanning mutagenesis of basic residue clusters, in vitro heparin binding assays, CXCR3 binding assays, in vitro and in vivo cell migration assays, NMR HSQC spectra The Journal of biological chemistry High 20363748
2005 CXCL11 has potent in vivo antitumor activity mediated primarily through recruitment of CD8+CXCR3+ T lymphocytes rather than inhibition of angiogenesis; in vivo CD8+ T cell depletion completely abolished the antitumor effect, and surviving mice developed protective antitumor immunity. EL4 tumor cells genetically modified to produce murine CXCL11, in vivo tumor growth assays, flow cytometric analysis of tumor infiltrates, in vivo CD8 T cell depletion, rechallenge experiments, IFN-γ production assays, angiogenesis assessment Journal of immunotherapy High 16000952
2014 CXCL11/CXCR3 engagement drives an immunotolerizing state (IL-10hi Tr1 and IL-4hi Th2 cells) via p70 kinase/mTOR in STAT3- and STAT6-dependent pathways, whereas CXCL10/CXCR3 drives effector Th1 polarization via STAT1, STAT4, and STAT5. A CXCL11-Ig fusion induced remission and prevented relapse in EAE mouse model. T cell polarization assays, phospho-STAT Western blots, mTOR pathway inhibitors, CXCL11-Ig fusion protein therapeutic study in SJL/J EAE model, GFP T cell trafficking assays The Journal of clinical investigation High 24713654
2005 CXCL11 attenuates bleomycin-induced pulmonary fibrosis by inhibiting angiogenesis and reducing pulmonary endothelial cell numbers; CXCR3 is not expressed on fibroblasts and CXCL11 has no direct effect on pulmonary fibroblasts, indicating the antifibrotic mechanism is indirect via vascular remodeling. In vivo bleomycin mouse model with systemic CXCL11 administration, collagen deposition assays, procollagen gene expression, histopathology, angiogenesis quantification, endothelial cell counting, CXCR3 expression analysis on fibroblasts American journal of respiratory and critical care medicine High 15502109
2012 CXCL10 and CXCL11 are allosteric ligands of CXCR3 that engage distinct receptor conformations: CXCR3 mutants D112N, D195N, and E196Q respond to CXCL11 but not CXCL10 or synthetic agonists, indicating CXCL11 recognition by CXCR3 is largely independent of D112 and extracellular loop residues D195/E196 required for CXCL10. CXCR3 point mutant generation, radioligand binding, chemotaxis assays with natural and synthetic ligands, molecular modelling British journal of pharmacology Medium 21895630
2016 ACKR3/CXCR7 binds CXCL11 through a different binding mode than CXCL12: CXCL11 requires the ACKR3 N-terminus and extracellular loop residues for primary binding and ECL residues for arrestin recruitment, while CXCL12 requires key residues D179 and D275 with no evident N-terminal involvement. Mutations reducing CXCL11 binding also impair scavenging; scavenging does not correlate with arrestin recruitment. 30 ACKR3 substitution mutants, radioligand competition binding, β-arrestin recruitment assays, chemokine scavenging assays The Journal of biological chemistry High 27875312
2005 CXCL9, CXCL10, and CXCL11 activate PI3K, MAPK, and actin reorganization in intestinal myofibroblasts through a Gαi-independent (pertussis toxin-insensitive) mechanism; CXCL11 uniquely elevates intracellular calcium in these cells despite no detectable surface CXCR3 expression, suggesting a variant or modified receptor coupling mechanism. PI3K and MAPK activation assays, actin reorganization assays, pertussis toxin treatment, calcium flux assays, CXCR3 surface expression analysis in intestinal myofibroblasts Journal of immunology Medium 16210647
2005 CXCL11-induced CXCR3-dependent cell migration requires the membrane proximal carboxyl terminus (including the LLL motif) for internalization and migration, and the third intracellular loop S245 for integrin-dependent adhesion, actin polymerization, and migration at high CXCL11 concentrations; pertussis toxin inhibits CXCL11-induced migration confirming Gαi dependence in HEK 293 cells. CXCR3 carboxyl-terminus and third intracellular loop mutants expressed in HEK 293 cells, migration assays, internalization assays, calcium flux, integrin adhesion assays, actin polymerization assays, pertussis toxin treatment Blood High 16368892
2008 EBV-encoded miRNA BHRF1-3 directly targets CXCL11/I-TAC mRNA; expression of BHRF1-3 inversely correlates with CXCL11 levels, and suppression of CXCL11 is reversed by transfection of antisense oligonucleotides to BHRF1-3. EBV miRNA expression profiling in primary lymphomas, inverse correlation analysis, antisense oligonucleotide rescue experiments Cancer research Medium 18316607
2005 IFN-beta preferentially inhibits osteoclastogenesis compared to IFN-alpha2 (100-fold more potent); expression profiling identified CXCL11 as the only gene differentially upregulated by IFN-beta, and recombinant CXCL11 alone inhibits osteoclastic differentiation, indicating CXCL11 mediates part of the anti-osteoclastogenic effect of IFN-beta via autocrine signaling. Monocyte osteoclastic differentiation assays, IFN-alpha vs. IFN-beta treatment comparison, genome-wide expression profiling, recombinant CXCL11 treatment of differentiating monocytes Proceedings of the National Academy of Sciences High 16081539
2006 CXCL11 promotes endometrial stromal cell proliferation via CXCR3 through p42/44 MAPK pathway activation, while inducing apoptosis of endometrial epithelial cells; IFN-gamma stimulates endometrial epithelial cells to produce CXCL11 which attracts trophoblast cells and T cells via CXCR3. Primary endometrial cell cultures, BrdU incorporation assays, lactate dehydrogenase release, annexin V staining, PD98059 MAPK inhibitor, immunoneutralization with anti-CXCL11 antibody, chemotaxis assays Journal of immunology Medium 17142784
2008 CXCL11 is secreted in a polarized basolateral-to-apical gradient by bronchial epithelial cells in COPD, driving T cell egression (transepithelial migration from interstitium to airway lumen) dependent on α4 and LFA-1 integrins, without requiring epithelial barrier disruption. Transepithelial resistance measurements, T cell migration assays across intact bronchial epithelium, integrin-blocking antibodies, CXCL11 localization by immunofluorescence, COPD patient biopsies Journal of immunology Medium 18209084
2008 CXCL11 (IP-9/I-TAC) produced by re-differentiating keratinocytes is required for wound repair: mice with antisense-mediated elimination of IP-9 expression during wound healing exhibit delayed re-epithelialization, hypercellular immature dermis, persistent provisional matrix components, and severely diminished basement membrane components (laminin V and collagen IV) without altered inflammatory response. Antisense transgenic mouse model (IP-9AS), full and partial thickness excisional wounds, histological analysis over 2 months, immunohistochemistry for matrix components The American journal of pathology High 18669615
2019 Docetaxel induces ROS-dependent HMGB1 release from tumor cells; HMGB1 then stimulates CXCL11 secretion via NF-κB activation, and CXCL11 enhances CD8+ T cell recruitment to the tumor microenvironment through CXCR3. Flow cytometry, immunofluorescence, Western blotting for HMGB1 and CXCL11, recombinant HMGB1 stimulation of CXCL11 production, ROS inhibition, NF-κB pathway analysis, in vivo CAR T cell recruitment assays Journal for immunotherapy of cancer Medium 30744691
2017 STAT2 regulates CXCL11 expression specifically in response to IFNα in keratinocytes; siRNA knockdown of STAT2 reduces IFNα-induced CXCL11 and CCL5 expression among 102 cytokines tested. This STAT2-dependent regulation of CXCL11 also requires IRF9 but not STAT1 or STAT6. STAT2 siRNA knockdown in human keratinocytes, 102-cytokine multiplex analysis, IFNα stimulation, IRF9/STAT1/STAT6 knockdown experiments PloS one Medium 28472186
2021 RBM15 enhances CXCL11 mRNA stability in an m6A-dependent manner in ccRCC cells; elevated RBM15 (driven by EP300/CBP-mediated histone acetylation of its promoter) increases CXCL11 secretion, which promotes macrophage infiltration and M2 polarization. RBM15 knockdown/overexpression, CXCL11 mRNA stability assays, m6A modification assays, ChIP for H3 acetylation, macrophage co-culture, in vivo xenograft models Free radical biology & medicine Medium 35381326
2018 Estrogen receptor α (ERα) directly binds the CXCR7 promoter in ovarian cancer cells to upregulate CXCR7 expression in response to estrogen; CXCL11 is also upregulated by estrogen, and CXCL11-induced ERα Ser-118 phosphorylation creates a positive feedback loop reinforcing CXCR7 transcription. CXCR7 (not CXCR3) mediates estrogen-induced mesenchymal marker expression and cancer cell migration. ChIP for ERα at CXCR7 promoter, histone modification analysis, CXCR7 siRNA knockdown, CXCL11-dependent ERα phosphorylation assays, cell migration assays, laser-capture microdissection of clinical samples Molecular oncology Medium 30051594
2015 The CXCR3-CXCL11 signaling axis mediates macrophage chemotaxis to bacterial infection sites in zebrafish; loss of the zebrafish CXCR3 ortholog (cxcr3.2) attenuates macrophage recruitment to infection foci, reduces granuloma formation, limits mycobacterial dissemination, and decreases bacterial burden. Recombinant CXCL11-like chemokines exert Cxcr3.2-dependent chemoattraction in vivo. Zebrafish cxcr3.2 mutant analysis, NBI74330 CXCR3 antagonist treatment, in vivo injection of recombinant CXCL11-like proteins, M. marinum infection model, macrophage migration imaging, granuloma quantification Disease models & mechanisms High 25573892
2007 IL-18 enhances IFN-γ-induced CXCL9, CXCL10, and CXCL11 production in human keratinocytes by activating NF-κB, STAT1, and IRF-1 through PI3K/Akt and MEK/ERK pathways; antisense oligonucleotides against NF-κB p50, p65, or STAT1 suppress CXCL11 production, and antisense IRF-1 specifically suppresses CXCL11. Cytokine stimulation of primary keratinocytes, ELISA, antisense oligonucleotides against transcription factors, PI3K/p38 MAPK/MEK inhibitors, phosphorylation assays European journal of immunology Medium 17274000
2019 CXCL11 promotes self-renewal, tumorigenic, and chemoresistance properties of α2δ1+ hepatocellular carcinoma tumor-initiating cells via ERK1/2 activation through CXCR3 in an autocrine manner, inducing stem cell-related genes BMI1, NANOG, MDR1, ABCG2, and CACNA2D1. CXCL11 stimulation of α2δ1+ HCC TICs, sphere formation assays, tumor initiation assays, ERK1/2 phosphorylation assays, CXCR3 receptor blocking, gene expression profiling of stemness markers Cancer letters Medium 30771435

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 CXCL9, CXCL10, CXCL11/CXCR3 axis for immune activation - A target for novel cancer therapy. Cancer treatment reviews 1157 29207310
2006 A novel chemokine receptor for SDF-1 and I-TAC involved in cell survival, cell adhesion, and tumor development. The Journal of experimental medicine 1069 16940167
1998 Interferon-inducible T cell alpha chemoattractant (I-TAC): a novel non-ELR CXC chemokine with potent activity on activated T cells through selective high affinity binding to CXCR3. The Journal of experimental medicine 690 9625760
2003 An alternatively spliced variant of CXCR3 mediates the inhibition of endothelial cell growth induced by IP-10, Mig, and I-TAC, and acts as functional receptor for platelet factor 4. The Journal of experimental medicine 587 12782716
2010 CXCR7 functions as a scavenger for CXCL12 and CXCL11. PloS one 388 20161793
1999 The T cell-specific CXC chemokines IP-10, Mig, and I-TAC are expressed by activated human bronchial epithelial cells. Journal of immunology (Baltimore, Md. : 1950) 301 10092813
2001 Differential expression of CXCR3 targeting chemokines CXCL10, CXCL9, and CXCL11 in different types of skin inflammation. The Journal of pathology 289 11523046
2000 Peroxisome proliferator-activated receptor-gamma activators inhibit IFN-gamma-induced expression of the T cell-active CXC chemokines IP-10, Mig, and I-TAC in human endothelial cells. Journal of immunology (Baltimore, Md. : 1950) 261 10843708
2008 EBV microRNAs in primary lymphomas and targeting of CXCL-11 by ebv-mir-BHRF1-3. Cancer research 259 18316607
2000 The ligands of CXC chemokine receptor 3, I-TAC, Mig, and IP10, are natural antagonists for CCR3. The Journal of biological chemistry 248 11110785
2010 Review: The chemokine receptor CXCR3 and its ligands CXCL9, CXCL10 and CXCL11 in neuroimmunity--a tale of conflict and conundrum. Neuropathology and applied neurobiology 237 20487305
2004 Intracellular domains of CXCR3 that mediate CXCL9, CXCL10, and CXCL11 function. The Journal of biological chemistry 215 15150261
2019 Cancer-cell-secreted CXCL11 promoted CD8+ T cells infiltration through docetaxel-induced-release of HMGB1 in NSCLC. Journal for immunotherapy of cancer 176 30744691
2022 CXCL11-armed oncolytic adenoviruses enhance CAR-T cell therapeutic efficacy and reprogram tumor microenvironment in glioblastoma. Molecular therapy : the journal of the American Society of Gene Therapy 167 36056553
2012 Chemokine receptor trio: CXCR3, CXCR4 and CXCR7 crosstalk via CXCL11 and CXCL12. Cytokine & growth factor reviews 164 22989616
2018 CXCL9, CXCL10, CXCL11, and their receptor (CXCR3) in neuroinflammation and neurodegeneration. Advances in clinical and experimental medicine : official organ Wroclaw Medical University 161 29893515
2014 CXCL11-dependent induction of FOXP3-negative regulatory T cells suppresses autoimmune encephalomyelitis. The Journal of clinical investigation 140 24713654
2007 IL-18 enhances IFN-gamma-induced production of CXCL9, CXCL10, and CXCL11 in human keratinocytes. European journal of immunology 140 17274000
2018 Intra-tumoral delivery of CXCL11 via a vaccinia virus, but not by modified T cells, enhances the efficacy of adoptive T cell therapy and vaccines. Oncoimmunology 135 29399394
2004 CXCL11 attenuates bleomycin-induced pulmonary fibrosis via inhibition of vascular remodeling. American journal of respiratory and critical care medicine 131 15502109
1999 Human IP-9: A keratinocyte-derived high affinity CXC-chemokine ligand for the IP-10/Mig receptor (CXCR3). The Journal of investigative dermatology 120 10233762
2020 Endothelial cells under therapy-induced senescence secrete CXCL11, which increases aggressiveness of breast cancer cells. Cancer letters 119 32659248
2005 The CXCR3 targeting chemokine CXCL11 has potent antitumor activity in vivo involving attraction of CD8+ T lymphocytes but not inhibition of angiogenesis. Journal of immunotherapy (Hagerstown, Md. : 1997) 118 16000952
2008 Citrullination of CXCL10 and CXCL11 by peptidylarginine deiminase: a naturally occurring posttranslational modification of chemokines and new dimension of immunoregulation. Blood 114 18645041
2015 The CXCR3-CXCL11 signaling axis mediates macrophage recruitment and dissemination of mycobacterial infection. Disease models & mechanisms 109 25573892
2021 Cancer-associated fibroblast-derived CXCL11 modulates hepatocellular carcinoma cell migration and tumor metastasis through the circUBAP2/miR-4756/IFIT1/3 axis. Cell death & disease 106 33707417
2003 CCR3 functional responses are regulated by both CXCR3 and its ligands CXCL9, CXCL10 and CXCL11. European journal of immunology 106 12884299
2021 The Pro-Inflammatory Chemokines CXCL9, CXCL10 and CXCL11 Are Upregulated Following SARS-CoV-2 Infection in an AKT-Dependent Manner. Viruses 105 34205098
2015 Blocking interferon γ reduces expression of chemokines CXCL9, CXCL10 and CXCL11 and decreases macrophage infiltration in ex vivo cultured arteries from patients with giant cell arteritis. Annals of the rheumatic diseases 98 26698852
2005 Interferon-alpha and -beta differentially regulate osteoclastogenesis: role of differential induction of chemokine CXCL11 expression. Proceedings of the National Academy of Sciences of the United States of America 98 16081539
2015 CXCL11-Armed oncolytic poxvirus elicits potent antitumor immunity and shows enhanced therapeutic efficacy. Oncoimmunology 96 27141352
2004 Expression of the CXCR3 ligand I-TAC by hepatocytes in chronic hepatitis C and its correlation with hepatic inflammation. Hepatology (Baltimore, Md.) 95 15122750
1999 The CXCR3 activating chemokines IP-10, Mig, and IP-9 are expressed in allergic but not in irritant patch test reactions. The Journal of investigative dermatology 95 10504443
2009 Monokine induced by interferon gamma (IFNgamma) (CXCL9) and IFNgamma inducible T-cell alpha-chemoattractant (CXCL11) involvement in Graves' disease and ophthalmopathy: modulation by peroxisome proliferator-activated receptor-gamma agonists. The Journal of clinical endocrinology and metabolism 90 19276231
2008 Matrix metalloproteinase processing of CXCL11/I-TAC results in loss of chemoattractant activity and altered glycosaminoglycan binding. The Journal of biological chemistry 84 18411283
2004 Synergistic induction of CXCL9 and CXCL11 by Toll-like receptor ligands and interferon-gamma in fibroblasts correlates with elevated levels of CXCR3 ligands in septic arthritis synovial fluids. Journal of leukocyte biology 75 14996826
2007 Prolactin enhances interferon-gamma-induced production of CXC ligand 9 (CXCL9), CXCL10, and CXCL11 in human keratinocytes. Endocrinology 71 17255201
2000 The murine chemokine CXCL11 (IFN-inducible T cell alpha chemoattractant) is an IFN-gamma- and lipopolysaccharide-inducible glucocorticoid-attenuated response gene expressed in lung and other tissues during endotoxemia. Journal of immunology (Baltimore, Md. : 1950) 70 10843686
2019 RNAseq Profiling of Leukocyte Populations in Zebrafish Larvae Reveals a cxcl11 Chemokine Gene as a Marker of Macrophage Polarization During Mycobacterial Infection. Frontiers in immunology 68 31110502
2010 CXCL9 and CXCL11 chemokines modulation by peroxisome proliferator-activated receptor-alpha agonists secretion in Graves' and normal thyrocytes. The Journal of clinical endocrinology and metabolism 63 20810571
2002 Dipeptidyl peptidase IV (CD26) on T cells cleaves the CXC chemokine CXCL11 (I-TAC) and abolishes the stimulating but not the desensitizing potential of the chemokine. Journal of leukocyte biology 63 12101279
2005 Interferon-inducible protein 9 (CXCL11)-induced cell motility in keratinocytes requires calcium flux-dependent activation of mu-calpain. Molecular and cellular biology 62 15713646
2002 A CXC chemokine sequence isolated from the rainbow trout Oncorhynchus mykiss resembles the closely related interferon-gamma-inducible chemokines CXCL9, CXCL10 and CXCL11. European cytokine network 62 12517732
2014 Cancer cell-derived lymphotoxin mediates reciprocal tumour-stromal interactions in human ovarian cancer by inducing CXCL11 in fibroblasts. The Journal of pathology 61 24014111
2013 Regulatory T cells, interleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), CXCL10, CXCL11, epidermal growth factor (EGF) and hepatocyte growth factor (HGF) as surrogate markers of host immunity in patients with renal cell carcinoma. BJU international 61 23495770
2022 Macrophage-derived CXCL9 and CXCL11, T-cell skin homing, and disease control in mogamulizumab-treated CTCL patients. Blood 60 34905599
2005 The chemokines CXCL9, CXCL10, and CXCL11 differentially stimulate G alpha i-independent signaling and actin responses in human intestinal myofibroblasts. Journal of immunology (Baltimore, Md. : 1950) 60 16210647
2006 The expression and possible roles of chemokine CXCL11 and its receptor CXCR3 in the human endometrium. Journal of immunology (Baltimore, Md. : 1950) 55 17142784
2010 Characterization of the chemokine CXCL11-heparin interaction suggests two different affinities for glycosaminoglycans. The Journal of biological chemistry 54 20363748
2022 Epigenetic activation of RBM15 promotes clear cell renal cell carcinoma growth, metastasis and macrophage infiltration by regulating the m6A modification of CXCL11. Free radical biology & medicine 52 35381326
2020 CXCL9, CXCL10, and CXCL11; biomarkers of pulmonary inflammation associated with autoimmunity in patients with collagen vascular diseases-associated interstitial lung disease and interstitial pneumonia with autoimmune features. PloS one 52 33137121
2014 Interaction of the chemokines I-TAC (CXCL11) and SDF-1 (CXCL12) in the regulation of tumor angiogenesis of colorectal cancer. Clinical & experimental metastasis 51 24493023
2019 CXCL11 promotes self-renewal and tumorigenicity of α2δ1+ liver tumor-initiating cells through CXCR3/ERK1/2 signaling. Cancer letters 49 30771435
2018 Upregulation of angiostatic chemokines IP-10/CXCL10 and I-TAC/CXCL11 in human obesity and their implication for adipose tissue angiogenesis. International journal of obesity (2005) 49 29795466
2015 Effect of JAK Inhibitors on Release of CXCL9, CXCL10 and CXCL11 from Human Airway Epithelial Cells. PloS one 49 26090665
2008 ELR-negative CXC chemokine CXCL11 (IP-9/I-TAC) facilitates dermal and epidermal maturation during wound repair. The American journal of pathology 46 18669615
2004 I-TAC/CXCL11 is a natural antagonist for CCR5. Journal of leukocyte biology 46 15178708
2019 The combination of CXCL9, CXCL10 and CXCL11 levels during primary HIV infection predicts HIV disease progression. Journal of translational medicine 44 31836011
2018 MiR-206 inhibits proliferation and migration of prostate cancer cells by targeting CXCL11. The Prostate 44 29542173
2016 Mutational Analysis of Atypical Chemokine Receptor 3 (ACKR3/CXCR7) Interaction with Its Chemokine Ligands CXCL11 and CXCL12. The Journal of biological chemistry 43 27875312
2007 Identification of CXCL11 as a STAT3-dependent gene induced by IFN. Journal of immunology (Baltimore, Md. : 1950) 42 17202361
2021 The role of anlotinib-mediated EGFR blockade in a positive feedback loop of CXCL11-EGF-EGFR signalling in anaplastic thyroid cancer angiogenesis. British journal of cancer 41 34088989
2020 Wrinkle in the plan: miR-34a-5p impacts chemokine signaling by modulating CXCL10/CXCL11/CXCR3-axis in CD4+, CD8+ T cells, and M1 macrophages. Journal for immunotherapy of cancer 41 33229509
2012 Small molecule chemokine mimetics suggest a molecular basis for the observation that CXCL10 and CXCL11 are allosteric ligands of CXCR3. British journal of pharmacology 40 21895630
2019 CXCL11 promotes tumor progression by the biased use of the chemokine receptors CXCR3 and CXCR7. Cytokine 38 31437604
2017 STAT2 is involved in the pathogenesis of psoriasis by promoting CXCL11 and CCL5 production by keratinocytes. PloS one 37 28472186
2015 Loss of RUNX3 expression promotes cancer-associated bone destruction by regulating CCL5, CCL19 and CXCL11 in non-small cell lung cancer. The Journal of pathology 37 26239696
2018 Down-regulation of CXCL11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition. OncoTargets and therapy 35 30425523
2020 CXCL11-CXCR3 Axis Mediates Tumor Lymphatic Cross Talk and Inflammation-Induced Tumor, Promoting Pathways in Head and Neck Cancers. The American journal of pathology 34 32035061
2005 Role of CXCR3 carboxyl terminus and third intracellular loop in receptor-mediated migration, adhesion and internalization in response to CXCL11. Blood 34 16368892
2004 Expression of interferon-inducible T cell alpha chemoattractant (CXCL11) in the salivary glands of patients with Sjögren's syndrome. Clinical immunology (Orlando, Fla.) 33 15308116
2004 Expression of rat I-TAC/CXCL11/SCYA11 during central nervous system inflammation: comparison with other CXCR3 ligands. Laboratory investigation; a journal of technical methods and pathology 33 15322564
2010 Integrating individual functional moieties of CXCL10 and CXCL11 into a novel chimeric chemokine leads to synergistic antitumor effects: a strategy for chemokine-based multi-target-directed cancer therapy. Cancer immunology, immunotherapy : CII 32 20706716
2018 Spinal CXCL9 and CXCL11 are not involved in neuropathic pain despite an upregulation in the spinal cord following spinal nerve injury. Molecular pain 31 29712506
2013 MIG (CXCL9), IP-10 (CXCL10) and I-TAC (CXCL11) concentrations after nasal allergen challenge in patients with allergic rhinitis. Archives of medical science : AMS 31 24273568
2021 CXCL11 Signaling in the Tumor Microenvironment. Advances in experimental medicine and biology 30 34286440
2019 Serum CXCL11 correlates with pulmonary outcomes and disease burden in sarcoidosis. Respiratory medicine 30 31128616
2018 Feedback control of the CXCR7/CXCL11 chemokine axis by estrogen receptor α in ovarian cancer. Molecular oncology 30 30051594
2004 NMR structure of CXCR3 binding chemokine CXCL11 (ITAC). Protein science : a publication of the Protein Society 30 15273303
1999 Induction of beta-R1/I-TAC by interferon-beta requires catalytically active TYK2. The Journal of biological chemistry 30 9890942
2016 PRMT5-Mediated Methylation of NF-κB p65 at Arg174 Is Required for Endothelial CXCL11 Gene Induction in Response to TNF-α and IFN-γ Costimulation. PloS one 29 26901772
2005 Adenovirus-directed ocular innate immunity: the role of conjunctival defensin-like chemokines (IP-10, I-TAC) and phagocytic human defensin-alpha. Investigative ophthalmology & visual science 29 16186347
2020 Effective Treatments for Bladder Cancer Affecting CXCL9/CXCL10/CXCL11/CXCR3 Axis: A Review. Oman medical journal 28 32181005
2017 Involvement of chemokine CXCL11 in the development of morphine tolerance in rats with cancer-induced bone pain. Journal of neurochemistry 26 27926984
2005 Synthesis of alpha-chemokines IP-10, I-TAC, and MIG are differentially regulated in human corneal keratocytes. Investigative ophthalmology & visual science 26 15851567
2021 Colon cancer cells secreted CXCL11 via RBP-Jκ to facilitated tumour-associated macrophage-induced cancer metastasis. Journal of cellular and molecular medicine 25 34655278
2015 Interleukin-27 and IFNγ regulate the expression of CXCL9, CXCL10, and CXCL11 in hepatitis. Journal of molecular medicine (Berlin, Germany) 25 26199110
2008 Polarized localization of epithelial CXCL11 in chronic obstructive pulmonary disease and mechanisms of T cell egression. Journal of immunology (Baltimore, Md. : 1950) 25 18209084
2022 CXCL8, CXCL9, CXCL10, and CXCL11 as biomarkers of liver injury caused by chronic hepatitis B. Frontiers in microbiology 24 36504808
2020 The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer. Cell death & disease 24 32341359
2013 Common structural interactions between the receptors CXCR3, CXCR4 and CXCR7 complexed with their natural ligands, CXCL11 and CXCL12, by a modeling approach. Cytokine 24 23773308
2021 Association of chemokines IP-10/CXCL10 and I-TAC/CXCL11 with insulin resistance and enhance leukocyte endothelial arrest in obesity. Microvascular research 23 34534571
2022 The LINC00152/miR-205-5p/CXCL11 axis in hepatocellular carcinoma cancer-associated fibroblasts affects cancer cell phenotypes and tumor growth. Cellular oncology (Dordrecht, Netherlands) 22 36435866
2006 Colon carcinoma cells induce CXCL11-dependent migration of CXCR3-expressing cytotoxic T lymphocytes in organotypic culture. Cancer immunology, immunotherapy : CII 21 16783574
2004 Glutamine and CXC chemokines IL-8, Mig, IP-10 and I-TAC in human intestinal epithelial cells. Clinical nutrition (Edinburgh, Scotland) 21 15297094
2018 Serum CXCL10, CXCL11, CXCL12, and CXCL14 chemokine patterns in patients with acute liver injury. Cytokine 20 29880273
2022 RAMP2-AS1 inhibits CXCL11 expression to suppress malignant phenotype of breast cancer by recruiting DNMT1 and DNMT3B. Experimental cell research 19 35390315
2019 Bu-Shen-Fang-Chuan formula attenuates T-lymphocytes recruitment in the lung of rats with COPD through suppressing CXCL9/CXCL10/CXCL11-CXCR3 axis. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 19 31864210
2023 Myostatin and CXCL11 promote nervous tissue macrophages to maintain osteoarthritis pain. Brain, behavior, and immunity 18 38070625
2019 The role of CXCR3 and its ligands CXCL10 and CXCL11 in the pathogenesis of celiac disease. Medicine 18 31232926