Affinage

CXCL11

C-X-C motif chemokine 11 · UniProt O14625

Length
94 aa
Mass
10.4 kDa
Annotated
2026-06-09
100 papers in source corpus 41 papers cited in narrative 41 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CXCL11 (I-TAC) is an IFN-inducible non-ELR CXC chemokine that orchestrates activated-T-cell trafficking and tissue remodeling by signaling through the receptor CXCR3, which it binds with higher affinity than the related ligands CXCL9 and CXCL10 (PMID:9625760, PMID:24713654). Through CXCR3 it triggers calcium mobilization and chemotaxis of IL-2-activated T cells, drives transendothelial migration, and is the principal physiological inducer of CXCR3 internalization on T cells contacting IFN-γ-activated endothelium (PMID:9625760, PMID:11739530). Receptor mutagenesis distinguishes CXCL11-specific signaling: its internalization uniquely requires the third intracellular loop and the membrane-proximal C-terminal LLL motif of CXCR3, whereas chemotaxis and calcium flux depend on the receptor C-terminus and the DRY motif and are pertussis-toxin sensitive (PMID:15150261, PMID:16368892). Biased CXCR3 signaling lets CXCL11 favor an immunotolerizing IL-10/IL-4 T-cell state via mTOR/STAT3/STAT6, in contrast to CXCL10-driven Th1 polarization, and a CXCL11-Ig fusion induces remission in EAE (PMID:24713654). Beyond CXCR3, CXCL11 binds ACKR3/CXCR7—which scavenges and degrades it through constitutive receptor cycling without G-protein signaling—and acts as a pure antagonist at CCR3 and CCR5 (PMID:11110785, PMID:15178708, PMID:16940167, PMID:20161793). CXCL11 activity is heavily controlled post-translationally: N-terminal truncation by DPP IV/CD26, CD13/aminopeptidase N, and MMP-8/9/12 abolishes agonism (converting it to a CXCR3 antagonist), C-terminal truncation removes the C-terminal-helix glycosaminoglycan-binding epitope required for in vivo gradient formation and cell recruitment, and PAD-mediated citrullination impairs signaling without altering CXCR3 binding (PMID:12101279, PMID:17363734, PMID:18411283, PMID:18645041, PMID:20363748). Transcriptionally, induction by type I/II IFNs requires TYK2 kinase activity, a non-canonical STAT3 function that recruits NF-κB p65 and IRF1 while displacing repressors, STAT2/IRF9 for IFN-α responses, and PRMT5-mediated p65 Arg174 methylation for TNF/IFN-γ costimulation (PMID:9890942, PMID:17202361, PMID:26901772, PMID:28472186). Functionally CXCL11 promotes keratinocyte motility through a PLC-β3/calcium/mu-calpain pathway and supports wound re-epithelialization and dermal maturation, inhibits osteoclastogenesis, attenuates pulmonary fibrosis by blocking angiogenesis rather than acting on fibroblasts, and recruits CD8+ T cells to mediate antitumor immunity (PMID:15713646, PMID:18669615, PMID:16081539, PMID:15502109, PMID:16000952).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1998 High

    Establishing that a new chemokine selectively engages CXCR3 defined CXCL11 as a dedicated recruiter of activated T cells rather than a broadly acting inflammatory mediator.

    Evidence Radioligand binding, calcium flux, and chemotaxis assays in activated T cells and CXCR3 transfectants

    PMID:10233762 PMID:9625760

    Open questions at the time
    • Cellular source range beyond T cells and keratinocytes not defined
    • Affinity ranking against other ligands quantified only later
  2. 1999 High

    Linking IFN-β-driven CXCL11 transcription to TYK2 kinase activity identified the first specific signaling requirement for its inducible expression.

    Evidence Complementation of TYK2-deficient cells with kinase-dead mutants plus CXCL11 promoter-reporter assay

    PMID:9890942

    Open questions at the time
    • Downstream transcription factors not yet mapped
    • TYK2 requirement specific to IFN-β not generalized to other inducers
  3. 2000 High

    Demonstrating that CXCL11 competitively blocks CCR3 without internalizing it revealed cross-receptor antagonism as a mechanism for restraining eosinophil/Th2 responses.

    Evidence Binding competition, chemotaxis, calcium, and internalization assays plus chimeric chemokine design on CCR3-bearing cells

    PMID:11110785 PMID:12884299

    Open questions at the time
    • In vivo relevance of CCR3 antagonism not established
    • Structural basis of antagonism only partially mapped via chimeras
  4. 2001 High

    Showing CXCL11 is the dominant inducer of CXCR3 internalization and transendothelial migration despite lower abundance established it as the functionally pre-eminent CXCR3 ligand at the endothelium.

    Evidence Immunofluorescence, flow cytometry, neutralizing antibodies, and pharmacological dissection on IFN-γ-activated endothelial co-cultures

    PMID:11739530

    Open questions at the time
    • Pertussis-toxin/wortmannin-insensitive internalization pathway not molecularly defined
  5. 2003 High

    Identifying CXCR3-B as a CXCL11 receptor on endothelium connected the chemokine to angiostatic and pro-apoptotic outcomes distinct from leukocyte chemotaxis.

    Evidence Splice-variant overexpression in HMEC-1 with binding, proliferation, and apoptosis readouts

    PMID:12782716

    Open questions at the time
    • Relative in vivo contribution of CXCR3-A vs CXCR3-B unresolved
    • Signaling effectors of CXCR3-B not detailed
  6. 2004 High

    Mutagenesis of CXCR3 dissected ligand-specific receptor domains, showing CXCL11 uses the third intracellular loop and C-terminal LLL motif for internalization separate from the shared chemotaxis machinery.

    Evidence Site-directed mutagenesis of CXCR3 intracellular domains with internalization, chemotaxis, calcium, adhesion, and pertussis-toxin assays

    PMID:15150261 PMID:16368892

    Open questions at the time
    • Adaptor proteins binding the third intracellular loop for CXCL11 not identified
  7. 2004 High

    Solving the CXCL11 NMR structure explained its monomeric, conformationally flexible behavior and set a structural basis for its multi-receptor and GAG interactions.

    Evidence Solution NMR spectroscopy with structural comparison to CXCL10

    PMID:15273303

    Open questions at the time
    • Functional consequence of monomeric state on receptor activation not resolved
  8. 2004 High

    Defining CXCL11 as a CCR5 antagonist extended its inhibitory cross-receptor repertoire and mapped residues responsible for CCR5 engagement.

    Evidence Binding competition, chemotaxis, calcium, and actin polymerization assays on CCR5 transfectants and monocytes with structural analysis

    PMID:15178708

    Open questions at the time
    • Physiological setting in which CCR5 antagonism operates not established
  9. 2005 High

    Identifying the PLC-β3/calcium/mu-calpain pathway clarified how CXCL11 drives keratinocyte motility distinct from growth-factor migration programs.

    Evidence In vitro wound healing, pharmacological inhibition, calpain isoform RNAi, FAK cleavage, and vinculin imaging

    PMID:15713646

    Open questions at the time
    • Whether the same pathway operates in T cells not tested
  10. 2005 Medium

    In vivo and ex vivo work attributed CXCL11's anti-fibrotic and antitumor effects to vascular remodeling and CD8 T-cell recruitment respectively, distinguishing direct from indirect tissue actions.

    Evidence Bleomycin pulmonary fibrosis model and CXCL11-expressing tumor model with CD8 depletion and angiogenesis analysis

    PMID:15502109 PMID:16000952

    Open questions at the time
    • Reconciliation of angiostatic vs T-cell-dependent mechanisms across tissues incomplete
    • Single-lab in vivo models
  11. 2006 High

    Showing CXCL11 binds CXCR7 without calcium/migration but conferring survival, and that GAG sequestration on endothelium controls its availability, revealed non-classical receptor and presentation mechanisms.

    Evidence CXCR7 binding/survival/adhesion assays plus heparin displacement and transendothelial migration in vivo

    PMID:16940167 PMID:16940188

    Open questions at the time
    • Heparin/GAG study confidence Medium; in vivo gradient mechanism inferred indirectly
  12. 2007 High

    Discovery of CD13/APN and synergistic CD26 N-terminal processing, plus STAT3-dependent promoter remodeling, defined both proteolytic inactivation and transcriptional control of CXCL11.

    Evidence Purified protease cleavage with binding/functional assays; STAT3-KO reconstitution with ChIP for p65/p50/IRF1/IRF2 at the CXCL11 promoter

    PMID:17202361 PMID:17274000 PMID:17363734

    Open questions at the time
    • Tissue contexts where each protease dominates not defined
    • Phosphorylation-independent STAT3 mechanism not fully explained
  13. 2008 High

    MMP processing and PAD citrullination established a layered post-translational code converting CXCL11 between agonist and antagonist and tuning GAG binding, while in vivo loss-of-function confirmed its wound-healing role.

    Evidence MS-mapped MMP-8/9/12 truncations with functional assays; PAD2 citrullination with binding/signaling/heparin assays; antisense CXCL11 transgenic mouse wound model

    PMID:18316607 PMID:18411283 PMID:18645041 PMID:18669615

    Open questions at the time
    • In vivo prevalence of citrullinated/truncated species not quantified
    • EBV miRNA target (idx 21) Medium confidence without direct 3'UTR validation
  14. 2010 High

    Defining CXCR7 as a non-saturable scavenger that degrades CXCL11 and mapping the C-terminal-helix/K17 GAG epitope required for in vivo migration established mechanisms controlling chemokine bioavailability and gradient formation.

    Evidence CXCR7 internalization/degradation/cycling assays in cells and zebrafish; alanine-scanning mutagenesis with heparin/CXCR3 binding and in vitro/in vivo migration plus NMR

    PMID:20161793 PMID:20363748

    Open questions at the time
    • Coupling between CXCR7 scavenging and CXCR3 signaling in vivo not fully integrated
  15. 2014 High

    Demonstrating biased CXCR3 signaling that drives immunotolerizing T cells positioned CXCL11 as a functional counterweight to CXCL10 and a candidate therapeutic in autoimmunity.

    Evidence STAT phosphorylation and T-cell polarization assays plus CXCL11-Ig therapy in relapsing EAE with in vivo T-cell tracking

    PMID:24713654

    Open questions at the time
    • Receptor conformational basis of biased signaling not structurally resolved
  16. 2016 High

    Mapping distinct ACKR3 binding modes for CXCL11 vs CXCL12 and PRMT5-dependent p65 Arg174 methylation refined both receptor engagement and the costimulatory transcriptional control of CXCL11.

    Evidence 30-mutant ACKR3 binding/arrestin/scavenging analysis; PRMT5 RNAi with p65 point-mutant reconstitution, MS, and ChIP at the CXCL11 promoter

    PMID:26901772 PMID:27875312

    Open questions at the time
    • Decoupling of arrestin recruitment from scavenging mechanistically unexplained
  17. 2019 Medium

    Tumor studies showed CXCL11/CXCR3-ERK signaling can be co-opted to promote cancer stemness and that chemotherapy induces CXCL11 to recruit CD8 T cells, casting CXCL11 as a context-dependent player in the tumor microenvironment.

    Evidence Recombinant CXCL11/CXCR3-blocking with ERK and sphere/tumorigenicity assays; docetaxel ROS→HMGB1→NF-κB→CXCL11 pathway with in vivo CAR-T infiltration

    PMID:30744691 PMID:30771435

    Open questions at the time
    • Single-lab studies
    • Pro- vs anti-tumor balance not resolved across cancer types
  18. 2021 Medium

    Identifying upstream regulators (RBM15/m6A stability, estrogen/ERα, AKT, CAF-derived circUBAP2 axis) expanded the transcriptional and post-transcriptional control network governing CXCL11 in disease.

    Evidence m6A stability assays, ChIP for ERα, AKT inhibitor in SARS-CoV-2-infected cells, and CAF co-culture with circRNA/miRNA dissection

    PMID:30051594 PMID:33707417 PMID:34205098 PMID:35381326

    Open questions at the time
    • AKT regulation (idx 36) Low confidence, inhibitor-only single cell line
    • Generalizability of these regulators beyond specific cancer models unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CXCL11's distinct receptor engagements (CXCR3-A/B, ACKR3, antagonized CCR3/CCR5) are integrated in vivo, and what determines its pro- versus anti-tumor and tolerizing versus inflammatory outcomes, remains unresolved.
  • No structural model of active CXCL11–CXCR3 complex in the timeline
  • Quantitative balance of scavenging vs signaling in tissues unknown
  • Determinants of context-dependent tumor outcomes undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 4 GO:0008289 lipid binding 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005576 extracellular region 3 GO:0005886 plasma membrane 2
Pathway
R-HSA-1500931 Cell-Cell communication 4 R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 4 R-HSA-74160 Gene expression (Transcription) 4
Partners
ACKR3CCR3CCR5CXCR3

Evidence

Reading pass · 41 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 selectively binds CXCR3 with higher affinity than the other CXCR3 ligands CXCL9 and CXCL10, induces transient intracellular calcium mobilization, and drives chemotactic migration of IL-2-activated T cells but not unstimulated T cells, neutrophils, or monocytes. Radioligand binding assays, calcium mobilization assays, chemotaxis assays using activated T cells and CXCR3-transfected cell lines The Journal of experimental medicine High 9625760
1999 CXCL11 (IP-9/beta-R1/H174/I-TAC) is a keratinocyte-derived CXCR3 ligand with a molecular mass of 8303 Da; it was isolated by challenging CXCR3-expressing CHO cells with IFN-γ-stimulated keratinocyte proteins and shown to be chemotactic for CXCR3-expressing activated T cells. Functional receptor activation assay on CXCR3-transfected CHO cells, protein purification, protein sequence analysis, mass spectrometry, molecular cloning of cDNA, chemotaxis assay The Journal of investigative dermatology High 10233762
1999 Induction of CXCL11 (beta-R1/I-TAC) by IFN-β requires catalytically active TYK2 kinase; cells with kinase-deficient TYK2 mutants fail to express CXCL11 in response to IFN-β despite robust induction of other IFN-stimulated genes, and this regulation occurs at the transcriptional level via the CXCL11 promoter. Complementation of TYK2-deficient U1 cells with wild-type or kinase-dead TYK2 mutants; transient transfection of CXCL11 promoter-reporter construct The Journal of biological chemistry High 9890942
2000 CXCL11 (I-TAC), along with CXCL9 and CXCL10, acts as a natural antagonist for CCR3: it competes for eotaxin binding to CCR3, inhibits CCR3-mediated migration and Ca²⁺ flux, and does not induce CCR3 internalization, qualifying it as a pure antagonist. A chimeric chemokine with the first 8 N-terminal residues of I-TAC substituted onto eotaxin showed enhanced CCR3 binding affinity. Radioligand binding competition assays on CCR3-bearing cells, chemotaxis assays, calcium mobilization assays, receptor internalization assays, chimeric chemokine design The Journal of biological chemistry High 11110785
2001 CXCL11 (I-TAC) is the principal physiological inducer of CXCR3 internalization upon T cell contact with IFN-γ-activated endothelial cells, despite being secreted at lower levels than CXCL10 or CXCL9; it is also the most potent inducer of transendothelial migration. CXCR3 internalization induced by CXCL11 is not blocked by pertussis toxin or wortmannin, suggesting a distinct signal transduction pathway from chemotaxis. Immunofluorescence microscopy, flow cytometry, neutralizing monoclonal antibodies to CXCL10/CXCL9/CXCL11, recombinant chemokine dose-response assays, transendothelial migration assay, pharmacological inhibitors Journal of immunology High 11739530
2002 DPP IV (CD26) expressed on T cells cleaves CXCL11 at its N-terminus (generating CXCL11(3-73)), reducing its CXCR3 binding affinity 8-fold, completely abolishing calcium flux and chemotactic activity, while retaining the ability to desensitize CXCR3 by down-regulating the receptor. DPP IV inhibitor, biochemical cleavage assay, radioligand binding, calcium flux assay, chemotaxis assay using PHA/IL-2-treated T cells Journal of leukocyte biology High 12101279
2003 CXCL11 signals through an alternatively spliced CXCR3 variant, CXCR3-B, which is expressed on microvascular endothelial cells and mediates angiostatic effects and apoptotic cell death, distinct from the pro-survival signaling of CXCR3-A. CXCL9, CXCL10, and CXCL11 all bind both CXCR3-A and CXCR3-B. Transfection of HMEC-1 cells with CXCR3-A or CXCR3-B constructs, radioligand binding, DNA synthesis assays, apoptosis assays, anti-CXCR3-B monoclonal antibodies, immunohistochemistry The Journal of experimental medicine High 12782716
2003 CXCL11 is the most efficacious antagonist of CCR3-mediated eosinophil responses among the CXCR3 ligands; it and other CXCR3 ligands share overlapping binding sites within the CCR3 extracellular loops (identified using CCR3-CCR1 chimeric receptor constructs), and CCL11 (eotaxin) binds CXCR3 with high affinity, suggesting CXCR3 may act as a decoy receptor for CCL11. Radioligand binding competition assays, calcium mobilization assays, chemotaxis assays using human eosinophils and CCR3 transfectants, CCR3-CCR1 chimeric receptor constructs European journal of immunology High 12884299
2004 CXCL11-induced CXCR3 internalization predominantly requires the third intracellular loop of CXCR3 (distinct from CXCL9/CXCL10 which require the C-terminal domain and beta-arrestin1); chemotaxis and calcium mobilization by all three ligands require the CXCR3 carboxyl terminus and the DRY motif in TM3. Site-directed mutagenesis of CXCR3 intracellular domains, internalization assays, chemotaxis assays, calcium mobilization assays in transfected cells The Journal of biological chemistry High 15150261
2004 CXCL11 (I-TAC) is a natural antagonist for CCR5: it inhibits MIP-1α binding to CCR5 transfectants and monocytes, and blocks RANTES- and MIP-1β-induced CCR5-mediated cell migration, intracellular calcium release, and actin polymerization. Sequence/structure analysis implicated residues K17, K49, and Q51 of CXCL11 in CCR5 binding. Radioligand binding competition assays on CCR5 transfectants and monocytes, chemotaxis assays, calcium mobilization, actin polymerization assay, structural analysis Journal of leukocyte biology High 15178708
2004 The NMR solution structure of CXCL11 (ITAC) adopts the canonical chemokine fold but exhibits greater conformational flexibility than related chemokines. Unlike CXCL10 and IL-8, CXCL11 does not form dimers at millimolar concentrations, attributable to a beta-bulge in beta-strand 1 that distorts the CXC dimerization interface. Solution NMR spectroscopy, structural comparison with CXCL10 Protein science High 15273303
2004 CXCL11-mediated CXCR3 internalization and cell migration require the membrane-proximal carboxyl terminus of CXCR3 (including the LLL motif specifically for CXCL11-induced internalization); integrin-dependent adhesion and actin polymerization at high CXCL11 concentrations require the third intracellular loop residue S245; migration is pertussis toxin-dependent. Site-directed mutagenesis of CXCR3 carboxyl terminus and third intracellular loop in HEK293 cells, internalization assays, migration assays, Ca²⁺ flux assays, integrin adhesion assays, pertussis toxin inhibition Blood High 16368892
2005 CXCL11 (IP-9) promotes motility in undifferentiated keratinocytes through CXCR3 signaling via a phospholipase C-β3/calcium flux/mu-calpain (calpain 1) pathway; it activates mu-calpain but not M-calpain (calpain 2), leading to cleavage of focal adhesion kinase and disassembly of vinculin aggregates, distinct from the ERK/M-calpain pathway used by EGF. In vitro wound healing assay, pharmacological inhibitors (PLC, calpain, calcium chelation), RNAi knockdown of calpain 1 vs. calpain 2, focal adhesion kinase cleavage assay, vinculin immunostaining, calpain activity assay Molecular and cellular biology High 15713646
2005 CXCL11 inhibits osteoclastic differentiation of human monocytes and mediates IFN-β's (but not IFN-α2's) superior inhibitory effect on osteoclastogenesis; CXCL11 is the only IFN-induced gene differentially upregulated by IFN-β relative to IFN-α2 in this system, and recombinant CXCL11 alone inhibits osteoclast differentiation. Expression profiling, recombinant CXCL11 treatment, osteoclast differentiation assays using primary human monocytes Proceedings of the National Academy of Sciences of the USA Medium 16081539
2006 CXCR7 binds CXCL11 (I-TAC) with high affinity in addition to its primary ligand CXCL12; unlike canonical chemokine receptors, CXCR7 activation by CXCL11 does not cause Ca²⁺ mobilization or induce cell migration, but confers a growth and survival advantage and increased cell adhesion. Radioligand binding assays, Ca²⁺ mobilization assay, migration assays, cell survival/growth assays, adhesion assays, small molecule CXCR7 antagonist in vivo tumor models The Journal of experimental medicine High 16940167
2006 Heparin displaces membrane-associated CXCL11 (I-TAC) from endothelial cell surfaces and reduces CXCL11-dependent transendothelial T cell migration, indicating that CXCL11 is sequestered on the vascular endothelium through glycosaminoglycan interactions; systemic heparin administration in vivo releases CXCL11 into plasma. In vivo heparin administration in cardiac surgery patients (plasma ELISA), displacement of membrane-associated chemokines from cultured endothelial cells, transendothelial migration assay under shear stress, in vivo T cell recruitment assay in humanized mouse model Circulation Medium 16940188
2007 CD13/aminopeptidase N (APN) processes CXCL11 by N-terminal truncation (removing up to 6 amino acids) to generate truncated forms that have reduced CXCR3 and CXCR7 binding and signaling, impaired lymphocyte chemotaxis, and failed calcium mobilization via CXCR3; truncated CXCL11 retains ability to desensitize CXCR3 but cannot induce Ca²⁺ flux through CXCR7. CD26/DPP IV also processes CXCL11 synergistically with CD13. Protease cleavage assays with purified CD13/APN and CD26, radioligand binding assays on CXCR3 and CXCR7 transfectants, calcium mobilization assays, chemotaxis assays with primary lymphocytes and transfected cells, HMVEC migration assay Blood High 17363734
2007 CXCL11 gene induction by IFN requires STAT3 in a manner independent of STAT3 Y705 phosphorylation; STAT3 recruits the transcriptional activators p65 (NF-κB) and IRF1 to the CXCL11 promoter, while displacing the repressors p50 and IRF2. In STAT3-deficient cells, p50 and IRF2 occupy the promoter instead. STAT3 knockout mouse embryonic fibroblasts reconstituted with wild-type or Y705 mutant STAT3, IFN sensitivity assays, chromatin immunoprecipitation (ChIP) assays for STAT3/p65/p50/IRF1/IRF2 binding to CXCL11 promoter Journal of immunology High 17202361
2007 IL-18 enhances IFN-γ-induced CXCL11 production in human keratinocytes through parallel activation of NF-κB, STAT1, and IRF-1; IRF-1 is specifically required for CXCL11 (but not CXCL9/CXCL10) production in this context. IL-18 activates PI3K/Akt and MEK/ERK pathways that regulate NF-κB and STAT1 activities. Antisense oligonucleotides against NF-κB p50, p65, STAT1, IRF-1; PI3K, p38 MAPK, MEK inhibitors; phosphorylation assays; ELISA and RT-PCR European journal of immunology Medium 17274000
2008 MMP-8 (PMN-specific), MMP-12 (macrophage-specific), and MMP-9 process CXCL11 at both N- and C-termini to generate CXCL11(5-73), (5-63), and (5-58). N-terminal truncation abolishes agonist activity and converts CXCL11 to a CXCR3 antagonist with enhanced heparin affinity; further C-terminal truncation to position 58 removes antagonist activity and heparin binding, revealing the C-terminal helix as critical for glycosaminoglycan binding. MALDI-TOF mass spectrometry substrate identification, recombinant MMP cleavage assays, calcium mobilization, chemotaxis assays using CXCR3 transfectants and human T lymphocytes, heparin binding assays The Journal of biological chemistry High 18411283
2008 Peptidylarginine deiminase (PAD/PAD2) citrullinates CXCL11 by deiminating arginine, impairing CXCR3 signaling and T-cell activation without affecting CXCR3 binding; citrullination also decreases heparin binding of CXCL11. PAD/PAD2 enzymatic treatment of CXCL11, CXCR3 binding assays, signaling assays, T-cell activation assays, heparin binding assays Blood High 18645041
2008 EBV miRNA BHRF1-3 suppresses CXCL11 (I-TAC) expression in lymphoma cells; transfection of an antisense oligonucleotide to BHRF1-3 reverses CXCL11 suppression, indicating CXCL11 is a direct target of this viral miRNA. Expression correlation analysis, antisense oligonucleotide reversal experiment in EBV-infected lymphoma cell lines Cancer research Medium 18316607
2008 CXCL11 (IP-9) produced by redifferentiating keratinocytes promotes re-epithelialization and dermal maturation during wound healing; mice expressing an antisense CXCL11 construct showed impaired wound healing with hypercellular immature dermis, delayed re-epithelialization, deficient basement membrane formation, and persistence of provisional matrix components. Antisense transgenic mouse model (IP-9AS), full and partial thickness excisional wounds, histological analysis over 2 months, immunostaining for laminin V, collagen IV The American journal of pathology High 18669615
2010 CXCR7 acts as a scavenger receptor for CXCL11 and CXCL12, mediating constitutive ligand internalization and targeting chemokines for degradation without G-protein coupling; CXCR7 continuously cycles between plasma membrane and intracellular compartments in the absence and presence of ligand, and CXCL11 scavenging is not saturable with increasing ligand concentrations. Chemokine internalization and degradation assays in mammalian cells and zebrafish, CXCR7 membrane cycling experiments, active CXCL12/CXCL11 sequestration demonstrated in mouse heart valves and human umbilical vein endothelium PloS one High 20161793
2010 GAG-binding epitopes of CXCL11 were mapped: residues in the C-terminal helix (K57SKQ AR62 cluster) together with K17 form the dominant heparin-binding epitope; mutation of these residues preserved near-wild-type CXCR3 binding and mild in vitro migration, but abolished in vivo cell migration, establishing a requirement for GAG binding for CXCL11 in vivo function. CXCL11 also exhibits conformational heterogeneity (NMR peak doubling) and more than one affinity state for both heparin and CXCR3. 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
2014 CXCL11/CXCR3 binding 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 Th1 polarization via STAT1/STAT4/STAT5 phosphorylation; CXCL11 binds CXCR3 with higher affinity than CXCL10. A CXCL11-Ig fusion molecule induced rapid remission and prevented relapse in EAE mice, mediated through reduced effector T cell accumulation at the autoimmune site. STAT phosphorylation assays (STAT1/3/4/5/6), T cell polarization assays, CXCL11-Ig fusion protein therapeutic treatment in relapsing EAE mouse model, GFP-expressing T cell tracking in vivo The Journal of clinical investigation High 24713654
2015 CXCR3-CXCL11 signaling axis controls macrophage recruitment to mycobacterial infections in zebrafish; CXCR3 (cxcr3.2) mutant zebrafish show attenuated macrophage chemotaxis to bacterial infections and reduced Mycobacterium marinum dissemination; recombinant CXCL11-like proteins exert Cxcr3.2-dependent chemoattraction in vivo; CXCR3 deficiency reduces granuloma formation and total bacterial burden. Zebrafish cxcr3.2 mutant model, CXCR3 antagonist NBI74330, in vivo macrophage chemotaxis assays, recombinant CXCL11-like protein local administration, Mycobacterium marinum infection model, granuloma quantification, bacterial burden assays Disease models & mechanisms High 25573892
2016 PRMT5-mediated symmetrical dimethylation of NF-κB p65 at Arg174 is required for CXCL11 gene induction by TNF-α plus IFN-γ costimulation in endothelial cells; p65 Arg174 methylation enhances p65 association with the CXCL11 promoter; this modification is distinct from Arg30/Arg35 methylation that controls CXCL10 induction. PRMT5 RNAi knockdown, p65 Arg174Ala/Lys reconstitution in p65-depleted endothelial cells, mass spectrometry of p65 methylation, ChIP and Re-ChIP assays for p65 and symmetrical dimethylarginine at CXCL11 promoter, CXCL11 mRNA/protein measurements PloS one High 26901772
2016 Comprehensive mutagenesis of ACKR3/CXCR7 reveals different binding modes for CXCL11 and CXCL12: CXCL11 binding depends on the ACKR3 N-terminus and extracellular loop (ECL) residues for primary binding with ECL residues mediating arrestin recruitment; CXCL12 requires key residues Asp179(4.60) and Asp275(6.58) without evident N-terminal involvement. Mutations reducing CXCL11 binding also diminish scavenging, but arrestin recruitment does not strictly correlate with scavenging. 30 substitution mutants of ACKR3, radioligand binding competition, beta-arrestin recruitment assays, chemokine scavenging assays The Journal of biological chemistry High 27875312
2017 STAT2, in conjunction with IRF9 (but not STAT1 or STAT6), is required for IFN-α-induced CXCL11 and CCL5 expression in human keratinocytes; gene silencing of STAT2 by siRNA identified CXCL11 as one of only two cytokines (out of 102 analyzed) regulated through this STAT2-dependent mechanism. siRNA silencing of STAT2 in human keratinocytes, 102-cytokine panel analysis, IFN-α stimulation, siRNA knockdown of STAT1, STAT6, IRF9 to identify pathway specificity PloS one Medium 28472186
2019 CXCL11 promotes self-renewal, tumorigenicity, and chemoresistance of α2δ1+ hepatocellular carcinoma tumor-initiating cells via CXCR3-mediated ERK1/2 activation, inducing stem cell-related genes (BMI1, NANOG, MDR1, ABCG2, CACNA2D1) through an autocrine signaling pathway. Recombinant CXCL11 treatment, CXCR3 blocking, ERK1/2 phosphorylation assays, sphere formation assays, tumorigenicity assays, gene expression analysis Cancer letters Medium 30771435
2019 Docetaxel induces CXCL11 secretion by cancer cells via an ROS-dependent HMGB1 release mechanism: DOC increases ROS, causing HMGB1 release; recombinant HMGB1 stimulates CXCL11 secretion through NF-κB activation; CXCL11 subsequently promotes CD8+ T cell recruitment to the tumor microenvironment. ROS measurement, HMGB1 release assay, recombinant HMGB1 + NF-κB inhibitor treatment, CXCL11 ELISA, in vivo DOC-treated mouse tumors with HER2-CAR T cell infiltration assay, flow cytometry, immunofluorescence, western blotting Journal for immunotherapy of cancer Medium 30744691
2020 CXCL11 secreted by therapy-induced senescent endothelial cells promotes breast cancer cell proliferation, migration, and invasion via CXCR3-mediated ERK activation; blocking CXCL11 with neutralizing antibody, CXCL11 siRNA, or CXCR3 siRNA synergistically reduces these effects. Conditioned medium transfer from senescent HUVEC, neutralizing anti-CXCL11 antibody, CXCL11 siRNA, CXCR3 siRNA, ERK phosphorylation assay, in vivo tumor-bearing mouse model Cancer letters Medium 32659248
2021 RBM15 enhances CXCL11 mRNA stability in an m6A-dependent manner in clear cell renal cell carcinoma cells, promoting CXCL11 secretion and thereby macrophage infiltration and M2 polarization; RBM15 expression itself is driven by EP300/CBP-mediated histone 3 acetylation of the RBM15 promoter. RBM15 overexpression/knockdown, m6A-dependent mRNA stability assays, ChIP for H3 acetylation at RBM15 promoter, CXCL11 ELISA, macrophage co-culture assays, in vivo mouse xenograft models Free radical biology & medicine Medium 35381326
2021 CXCL11 promotes HCC cell migration through a CXCR3/ERK1/2 signaling pathway; cancer-associated fibroblast (CAF)-derived CXCL11 activates the circUBAP2/miR-4756/IFIT1/3 axis in tumor cells, upregulating IL-1β and IL-17 to enhance migration; CXCL11 stimulation upregulates circUBAP2, which sponges miR-4756 to relieve inhibition of IFIT1 and IFIT3. CAF co-culture and conditioned medium assays, CXCL11 siRNA in CAFs, circUBAP2 silencing, IFIT1/IFIT3 silencing, miR-4756 inhibitor, IL-17/IL-1β measurements, in vivo orthotopic tumor models with metastasis quantification Cell death & disease Medium 33707417
2018 Estrogen receptor α (ERα) directly recruits to and activates the CXCR7 promoter in ovarian cancer cells in response to estrogen, and CXCL11 gene expression is also upregulated by estrogen, causing Ser-118 phosphorylation and activation of ERα for positive feedback regulation of the CXCR7 promoter; CXCR7 (not CXCR3) mediates estrogen-induced mesenchymal marker expression and cancer cell migration. ChIP for ERα and histone modifications at CXCR7 promoter, CXCR7 expression knockdown, CXCL11 siRNA, cell migration assays, mesenchymal marker expression assays, ERα Ser-118 phosphorylation assays, microdissected tumor analysis Molecular oncology Medium 30051594
2021 CXCL11 upregulation in response to SARS-CoV-2 infection in human lung epithelial cells is mediated in an AKT-dependent manner; pharmacological inhibition of AKT (GSK690693) markedly reduces CXCL11 gene induction, implicating the AKT pathway as a regulatory node for CXCL11 transcription during viral infection. SARS-CoV-2 infection of Calu-3 cells, small molecule kinase inhibitors (including AKT inhibitor GSK690693), qRT-PCR of CXCL11 transcripts Viruses Low 34205098
2005 CXCL11 exerts its antitumor activity in vivo exclusively through attraction of CD8+CXCR3+ T lymphocytes, not through inhibition of angiogenesis; CD8 T cell depletion completely abrogated tumor rejection, and survivors developed tumor-specific IFN-γ-producing CD8+ T cell memory. EL4 tumor cells genetically modified to produce murine CXCL11, in vivo tumor growth assay, flow cytometry of tumor infiltrate, in vivo CD8 T cell depletion, angiogenesis analysis, rechallenge experiments with IFN-γ ELISpot Journal of immunotherapy Medium 16000952
2004 CXCL11 attenuates bleomycin-induced pulmonary fibrosis by inhibiting aberrant vascular remodeling (reducing angiogenesis and endothelial cell numbers) rather than by directly affecting fibroblasts (CXCR3 is not expressed on fibroblasts and CXCL11 has no direct functional effect on pulmonary fibroblasts). Systemic CXCL11 administration in bleomycin mouse model, measurement of collagen deposition, procollagen gene expression, histopathology, lung leukocyte populations, angiogenic activity, endothelial cell quantification American journal of respiratory and critical care medicine Medium 15502109
2008 CXCL11 drives T cell egression (luminal clearance) across bronchial epithelium through a polarized transepithelial gradient; T cell adhesion to the basal surface requires α4 integrin and LFA-1, and transmigration is LFA-1-dependent; egression decreases transepithelial resistance without grossly altering tight-junction proteins and does not require epithelial injury. T cell egression assay across primary bronchial epithelium, CXCL11 gradient assay, integrin blocking antibodies (anti-α4, anti-LFA-1), transepithelial resistance measurement, immunofluorescence for tight-junction proteins Journal of immunology Medium 18209084
2005 CXCL9, CXCL10, and CXCL11 stimulate Gαi-independent PI3K/MAPK activation and actin reorganization in intestinal myofibroblasts (CXCR3 mRNA detectable but no surface CXCR3 detected); CXCL11 uniquely elevates intracellular calcium in these cells. These responses are pertussis-toxin insensitive, suggesting a modified or variant CXCR3 coupling mechanism distinct from peripheral blood lymphocytes. PI3K and MAPK activation assays, actin reorganization assays, calcium mobilization assay, RT-PCR and flow cytometry for CXCR3 expression, pertussis toxin inhibition Journal of immunology Medium 16210647

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 1199 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 1072 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 694 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 590 12782716
2010 CXCR7 functions as a scavenger for CXCL12 and CXCL11. PloS one 391 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
2008 EBV microRNAs in primary lymphomas and targeting of CXCL-11 by ebv-mir-BHRF1-3. Cancer research 262 18316607
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
2000 The ligands of CXC chemokine receptor 3, I-TAC, Mig, and IP10, are natural antagonists for CCR3. The Journal of biological chemistry 249 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 218 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 175 36056553
2018 CXCL9, CXCL10, CXCL11, and their receptor (CXCR3) in neuroinflammation and neurodegeneration. Advances in clinical and experimental medicine : official organ Wroclaw Medical University 166 29893515
2012 Chemokine receptor trio: CXCR3, CXCR4 and CXCR7 crosstalk via CXCL11 and CXCL12. Cytokine & growth factor reviews 165 22989616
2014 CXCL11-dependent induction of FOXP3-negative regulatory T cells suppresses autoimmune encephalomyelitis. The Journal of clinical investigation 143 24713654
2007 IL-18 enhances IFN-gamma-induced production of CXCL9, CXCL10, and CXCL11 in human keratinocytes. European journal of immunology 141 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 138 29399394
2004 CXCL11 attenuates bleomycin-induced pulmonary fibrosis via inhibition of vascular remodeling. American journal of respiratory and critical care medicine 131 15502109
2020 Endothelial cells under therapy-induced senescence secrete CXCL11, which increases aggressiveness of breast cancer cells. Cancer letters 122 32659248
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
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
2001 CXCR3 internalization following T cell-endothelial cell contact: preferential role of IFN-inducible T cell alpha chemoattractant (CXCL11). Journal of immunology (Baltimore, Md. : 1950) 118 11739530
2007 Proteolytic processing of CXCL11 by CD13/aminopeptidase N impairs CXCR3 and CXCR7 binding and signaling and reduces lymphocyte and endothelial cell migration. Blood 116 17363734
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 112 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 110 33707417
2003 CCR3 functional responses are regulated by both CXCR3 and its ligands CXCL9, CXCL10 and CXCL11. European journal of immunology 108 12884299
2021 The Pro-Inflammatory Chemokines CXCL9, CXCL10 and CXCL11 Are Upregulated Following SARS-CoV-2 Infection in an AKT-Dependent Manner. Viruses 106 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 101 26698852
2015 CXCL11-Armed oncolytic poxvirus elicits potent antitumor immunity and shows enhanced therapeutic efficacy. Oncoimmunology 100 27141352
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
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 76 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
2002 Expression and modulation of IFN-gamma-inducible chemokines (IP-10, Mig, and I-TAC) in human brain endothelium and astrocytes: possible relevance for the immune invasion of the central nervous system and the pathogenesis of multiple sclerosis. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 64 12162873
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
2022 Macrophage-derived CXCL9 and CXCL11, T-cell skin homing, and disease control in mogamulizumab-treated CTCL patients. Blood 61 34905599
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
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
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 55 33137121
2010 Characterization of the chemokine CXCL11-heparin interaction suggests two different affinities for glycosaminoglycans. The Journal of biological chemistry 55 20363748
2006 Heparin displaces interferon-gamma-inducible chemokines (IP-10, I-TAC, and Mig) sequestered in the vasculature and inhibits the transendothelial migration and arterial recruitment of T cells. Circulation 55 16940188
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
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 53 35381326
2015 Effect of JAK Inhibitors on Release of CXCL9, CXCL10 and CXCL11 from Human Airway Epithelial Cells. PloS one 53 26090665
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
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) 50 29795466
2019 CXCL11 promotes self-renewal and tumorigenicity of α2δ1+ liver tumor-initiating cells through CXCR3/ERK1/2 signaling. Cancer letters 49 30771435
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 44 27875312
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 42 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 42 33229509
2007 Identification of CXCL11 as a STAT3-dependent gene induced by IFN. Journal of immunology (Baltimore, Md. : 1950) 42 17202361
2017 STAT2 is involved in the pathogenesis of psoriasis by promoting CXCL11 and CCL5 production by keratinocytes. PloS one 39 28472186
2019 CXCL11 promotes tumor progression by the biased use of the chemokine receptors CXCR3 and CXCR7. Cytokine 38 31437604
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
2002 IFN-gamma regulates murine interferon-inducible T cell alpha chemokine (I-TAC) expression in dendritic cell lines and during experimental autoimmune encephalomyelitis (EAE). Scandinavian journal of immunology 37 11896933
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 35 32035061
2018 Down-regulation of CXCL11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition. OncoTargets and therapy 35 30425523
2019 Serum CXCL11 correlates with pulmonary outcomes and disease burden in sarcoidosis. Respiratory medicine 34 31128616
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 rat I-TAC/CXCL11/SCYA11 during central nervous system inflammation: comparison with other CXCR3 ligands. Laboratory investigation; a journal of technical methods and pathology 34 15322564
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
2005 Increased expression of CXCR3 and CCR5 on memory CD4+ T-cells migrating into the cerebrospinal fluid of patients with neuroborreliosis: the role of CXCL10 and CXCL11. Journal of neuroimmunology 32 15885315
2021 CXCL11 Signaling in the Tumor Microenvironment. Advances in experimental medicine and biology 31 34286440
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
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
2011 Chemokine CXCL11 links microbial stimuli to intestinal inflammation. Clinical and experimental immunology 29 21438871
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
2021 Colon cancer cells secreted CXCL11 via RBP-Jκ to facilitated tumour-associated macrophage-induced cancer metastasis. Journal of cellular and molecular medicine 26 34655278
2005 Synthesis of alpha-chemokines IP-10, I-TAC, and MIG are differentially regulated in human corneal keratocytes. Investigative ophthalmology & visual science 26 15851567
2022 CXCL8, CXCL9, CXCL10, and CXCL11 as biomarkers of liver injury caused by chronic hepatitis B. Frontiers in microbiology 25 36504808
2020 The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer. Cell death & disease 25 32341359
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
2021 Association of chemokines IP-10/CXCL10 and I-TAC/CXCL11 with insulin resistance and enhance leukocyte endothelial arrest in obesity. Microvascular research 24 34534571
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
2009 Modelling of the membrane receptor CXCR3 and its complexes with CXCL9, CXCL10 and CXCL11 chemokines: putative target for new drug design. Molecular immunology 24 19800124
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) 23 36435866
2010 Role of I-TAC-binding receptors CXCR3 and CXCR7 in proliferation, activation of intracellular signaling pathways and migration of various tumor cell lines. Folia histochemica et cytobiologica 21 20529825
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

Missed literature

Know a paper Affinage missed for CXCL11? Flag it for the maintainers and the community.

No submissions yet.