Affinage

IL13

Interleukin-13 · UniProt P35225

Round 2 corrected
Length
146 aa
Mass
15.8 kDa
Annotated
2026-04-28
130 papers in source corpus 39 papers cited in narrative 38 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

IL-13 is a pleiotropic Th2 cytokine that orchestrates type 2 immune responses, tissue remodeling, and repair across multiple organ systems. It signals canonically through the type II receptor complex (IL-4Rα/IL-13Rα1), activating STAT6 to drive IgE class switching in B cells, goblet cell metaplasia via MAPK/PI3K cascades, airway hyperresponsiveness through enhanced smooth muscle calcium signaling, alternative macrophage activation including catecholamine production for beige fat biogenesis, and epithelial barrier remodeling (PMID:9856949, PMID:8097324, PMID:12794003, PMID:24906148, PMID:24220297). A parallel signaling axis through IL-13Rα2 activates AP-1 (c-jun/Fra-2) to induce TGF-β1 transcription and a downstream fibrogenic cascade involving IGF-I and Egr-1, establishing IL-13Rα2 as a bona fide signaling receptor rather than merely a decoy (PMID:16327802, PMID:18938165). IL-13 bioavailability and signaling are regulated at multiple levels, including post-transcriptional repression by let-7 miRNAs, miR-155-mediated targeting of IL-13Rα1, MMP-8-dependent shedding of soluble IL-13Rα2, Akt1-dependent production in macrophages, and a cooperative requirement for apoptotic cell recognition to activate the full tissue repair program (PMID:21616524, PMID:21097505, PMID:18694590, PMID:28495875).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1993 High

    Identification of IL-13 as a novel T cell-derived cytokine that suppresses monocyte inflammatory cytokines, induces B cell proliferation and IgE class switching independently of IL-4, and maps to chromosome 5q31 near IL-4 established IL-13 as a non-redundant Th2 effector cytokine.

    Evidence cDNA cloning from activated T cells, recombinant protein functional assays on monocytes and B cells, anti-IL-4 neutralization demonstrating IL-4-independent IgE switching

    PMID:7688562 PMID:8096327 PMID:8097324

    Open questions at the time
    • Receptor identity and signaling pathway unknown
    • In vivo relevance of IL-13 in disease not yet tested
    • Relationship to IL-4 at the receptor level undefined
  2. 1998 High

    Demonstration that IL-13 is both necessary and sufficient for hallmark asthma features (airway hyperresponsiveness, mucus overproduction) independently of IgE and eosinophils, and is non-redundantly required for intestinal helminth expulsion, established IL-13 as a central effector of allergic and anti-helminth immunity in vivo.

    Evidence Selective IL-13 neutralization and IL-13 KO mice in asthma and Trichuris muris infection models; IL-4Rα-deficient mice

    PMID:9531306 PMID:9856949 PMID:9856950

    Open questions at the time
    • Precise epithelial signaling mechanism for mucus induction unknown
    • Relative contributions of IL-13Rα1 versus IL-13Rα2 in vivo unclear
    • Molecular basis of airway smooth muscle hyperresponsiveness not defined
  3. 2001 High

    Elucidation of downstream epithelial effector mechanisms showed IL-13 drives mucus overproduction through EGFR/neutrophil-dependent and MAPK/PI3K pathways, alters mucociliary differentiation via IL-4Rα, and requires STAT6 for airway hyperreactivity, defining the intracellular signaling architecture in target tissues.

    Evidence EGFR inhibitors, neutrophil depletion, and kinase inhibitors in vivo and in air-liquid interface epithelial cultures; STAT6-KO and IL-4Rα-KO mice with allergen challenge

    PMID:11133503 PMID:11466392 PMID:11748265 PMID:12794003

    Open questions at the time
    • Whether EGFR-dependent and MAPK/PI3K-dependent mucus pathways are cell-type specific or context dependent
    • STAT6-independent IL-13 signaling components not identified
    • Mechanism of IL-13 action on smooth muscle contractility only partially defined
  4. 2003 High

    IL-13 was shown to directly enhance airway smooth muscle contractility and calcium signaling, and to suppress iNOS in macrophages via arginase-mediated arginine depletion, revealing cell-type-specific effector mechanisms beyond epithelial targets.

    Evidence Tracheal ring contractility and calcium fluorimetry in human ASM cells; arginase inhibitors and metabolic labeling in primary macrophages

    PMID:14568929 PMID:14597600

    Open questions at the time
    • In vivo relevance of direct smooth muscle signaling versus indirect epithelial effects unresolved
    • Whether arginase-mediated translational control extends to other IL-13 target proteins unknown
  5. 2005 High

    Discovery that IL-13Rα2 functions as a signaling receptor activating AP-1 (c-jun/Fra-2) to induce TGF-β1 and drive fibrosis overturned the prevailing decoy-only model, while characterization of the R130Q variant revealed reduced IL-13Rα2 decoy function and enhanced STAT6 signaling as a mechanism for genetic asthma risk.

    Evidence AP-1 promoter analysis, IL-13Rα2 siRNA in colitis/fibrosis models; recombinant WT vs R130Q protein binding and signaling assays on primary human cells with patient serum correlation

    PMID:12063528 PMID:15711639 PMID:16327802

    Open questions at the time
    • Crystal structure of IL-13/IL-13Rα2 signaling complex not available at this time
    • Full spectrum of IL-13Rα2-dependent transcriptional targets beyond TGF-β1 undefined
    • How IL-13Rα2 signaling versus decoy functions are balanced in different tissues unclear
  6. 2007 High

    Multiple upstream triggers and feedback mechanisms were identified: IL-33 induces IL-13 from mast cells via MyD88, IL-9 requires IL-13 as a downstream mediator for lung eosinophilia, epithelial injury triggers autocrine IL-13/HB-EGF/EGFR repair signaling with negative feedback, and IL-13 activates PPARγ for CD36-mediated phagocytosis in monocytes.

    Evidence MyD88-KO mast cells, IL-13-KO × IL-9-transgenic mice, scratch wound assays with IL-13 neutralization, PPARγ-null macrophages with PLA2 inhibitors

    PMID:17312173 PMID:17458857 PMID:17717322 PMID:17881510

    Open questions at the time
    • Whether IL-33→IL-13 axis operates equivalently across all tissue-resident mast cell populations
    • Full extent of autocrine IL-13 signaling in non-airway epithelia unclear
    • PPARγ-mediated CD36 pathway not tested beyond malaria phagocytosis
  7. 2008 High

    Structural resolution of the complete type II receptor ternary complexes revealed that IL-13 engages IL-13Rα1 through a novel top-mounted Ig-like domain with recognition chemistry distinct from IL-4, while MMP-8 was identified as a protease that sheds IL-13Rα2 to regulate IL-13 bioavailability in vivo, and IL-13Rα2-driven fibrosis was shown to involve a multi-step cascade (TGF-β1, IGF-I, Egr-1).

    Evidence X-ray crystallography of IL-4Rα/IL-13Rα1/IL-13 ternary complexes; MMP-8-KO mice with allergen challenge; siRNA knockdown of IL-13Rα2/TGF-β1 pathway components in chronic colitis

    PMID:18243101 PMID:18694590 PMID:18938165

    Open questions at the time
    • Structure of IL-13/IL-13Rα2 signaling complex not resolved
    • Other proteases that may regulate IL-13Rα2 shedding not identified
    • Structural basis for differential STAT6 activation potency by IL-4 vs IL-13 incompletely explained
  8. 2010 High

    Post-transcriptional and post-signaling regulatory layers were defined: miR-155 directly targets IL-13Rα1 to attenuate STAT6-dependent M2 macrophage polarization, IL-13 drives alternative macrophage activation for catecholamine-dependent beige fat biogenesis, and IL-13 disrupts epithelial barrier integrity by downregulating desmoglein-1 in eosinophilic esophagitis.

    Evidence miR-155 luciferase reporter assays in primary macrophages; IL-4/IL-13-signaling-deficient mice under cold stress; DSG1 siRNA and transepithelial resistance in esophageal epithelial cells with patient biopsy validation

    PMID:21097505 PMID:24220297 PMID:24906148

    Open questions at the time
    • Whether miR-155 regulation of IL-13Rα1 varies across tissue macrophage populations unknown
    • The catecholamine-producing macrophage pathway has been debated regarding reproducibility in other mouse strains
    • Mechanism linking IL-13 to DSG1 transcriptional downregulation not fully defined
  9. 2011 Medium

    Let-7 miRNAs were shown to directly repress IL-13 mRNA, and intranasal let-7 delivery resolved allergic airway disease features, establishing post-transcriptional control of IL-13 itself as a regulatory node.

    Evidence Bioinformatic prediction, in vitro transfection in T cells, intranasal let-7 mimic in murine allergy model

    PMID:21616524

    Open questions at the time
    • Endogenous regulation of let-7 levels in Th2 cells during allergic inflammation not defined
    • Specificity of let-7 for IL-13 versus other Th2 cytokines at endogenous expression levels not resolved
  10. 2017 High

    An IL-33→IL-13 signaling cascade was shown to be required for spasmolytic polypeptide-expressing metaplasia after parietal cell loss, full macrophage tissue repair programming requires IL-13 together with apoptotic cell recognition (neither alone suffices), and autophagy was identified as required for IL-13-induced apical DUOX1 localization and superoxide production.

    Evidence IL-33/ST2/IL-13 triple KO epistasis with IL-13 rescue in gastric metaplasia model; genetic ablation of apoptotic cell sensors in helminth and colitis models; ATG5/DUOX1 siRNA in airway epithelial cells with EPR spectroscopy

    PMID:28196875 PMID:28495875 PMID:28982074

    Open questions at the time
    • Identity of the apoptotic cell sensor cooperating with IL-13 signaling not fully defined
    • Whether the IL-33→IL-13 metaplasia pathway operates in human gastric disease untested
    • How autophagy specifically directs DUOX1 trafficking versus general cargo unclear
  11. 2019 High

    ILC2-derived IL-13 was shown to maintain intestinal stem cell self-renewal via circPan3-stabilized IL-13Rα1/Foxp1/β-catenin signaling, Treg-derived IL-13 was demonstrated to be protective in acute lung injury by restraining monocyte accumulation, and Akt1 was identified as a kinase regulating macrophage IL-13 production and pulmonary fibrosis susceptibility.

    Evidence circPan3 deletion in Lgr5+ ISCs with RNA-protein interaction and Foxp1-β-catenin co-IP; Foxp3Cre × Il4/Il13 floxed mice in lung injury; Akt1-KO macrophages with IL-33 stimulation and bleomycin fibrosis model

    PMID:30643264 PMID:30779711 PMID:31299858

    Open questions at the time
    • Whether circPan3-IL-13Rα1 axis operates in other stem cell niches unknown
    • Human relevance of Treg-derived IL-13 in ARDS or lung injury not tested
    • Akt1 substrates directly linking to IL-13 transcription/secretion not identified
  12. 2021 High

    Eosinophil-derived IL-13 produced via ST2 signaling was shown to mediate hepatoprotection against ischemia-reperfusion injury, extending the tissue-protective role of cell-type-specific IL-13 beyond the lung.

    Evidence Genetic eosinophil-deficient mice, adoptive transfer of WT vs ST2-KO eosinophils, liver IRI model with biochemical and histological assessment

    PMID:33536281

    Open questions at the time
    • Downstream hepatic targets of eosinophil-derived IL-13 not identified
    • Whether IL-13Rα2-mediated fibrogenic signaling is engaged in hepatic IRI context unclear
    • Therapeutic window and translational relevance of eosinophil IL-13 in human liver IRI unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of IL-13Rα2 signaling (vs decoy) complex formation, how tissue-specific receptor expression ratios determine fibrotic vs protective outcomes, and the therapeutic implications of selectively blocking IL-13Rα2 signaling while preserving IL-13Rα1-mediated repair.
  • No crystal structure of IL-13/IL-13Rα2 signaling complex available
  • Integrated quantitative model of IL-13 signal partitioning between Rα1 and Rα2 across tissues lacking
  • Cell-type-specific functions of IL-13 from distinct immune sources (ILC2, Treg, eosinophil, Th2) not systematically compared

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 4 GO:0098772 molecular function regulator activity 3
Localization
GO:0005576 extracellular region 5
Pathway
R-HSA-168256 Immune System 10 R-HSA-162582 Signal Transduction 6 R-HSA-1643685 Disease 6
Partners
CHI3L1IL13RA1IL13RA2IL33IL4RSTAT6

Evidence

Reading pass · 38 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 IL-13 was identified as a new human cytokine expressed in activated T lymphocytes, capable of inhibiting inflammatory cytokine production induced by LPS in human peripheral blood monocytes, and its gene was mapped to chromosome 5q23-31, closely linked to the IL-4 gene. Differential screening of subtracted cDNA library, recombinant protein expression, functional assays on monocytes Nature High 8096327
1993 Human IL-13 protein induces morphological changes in human monocytes with upregulation of MHC class II antigens and CD23 (Fc epsilon RII), stimulates proliferation of anti-IgM or anti-CD40-activated human B cells, and induces IgM and IgG (but not IgA) production by purified B cells co-cultured with activated CD4+ T cells. cDNA cloning, recombinant protein expression, B cell proliferation assays, Ig production assays, flow cytometry Proceedings of the National Academy of Sciences of the United States of America High 8097324
1993 IL-13 synergizes with mouse and human CD40L to induce IgM, IgG, IgG4, and IgE (but not IgA) production by highly purified B cells, and this induction is independent of IL-4 (anti-IL-4 antibodies block IL-4-induced but not IL-13-induced Ig production), demonstrating that IL-13 and CD40L can induce isotype switching to IgE independently of IL-4. B cell-T cell co-culture, COS-7 cells transfected with hCD40L, neutralizing antibody blockade, ELISA International immunology High 7688562
1998 IL-13 is necessary and sufficient for the expression of allergic asthma features (airway hyperresponsiveness, mucus overproduction) in a manner independent of IgE and eosinophils; selective neutralization of IL-13 ameliorated the asthma phenotype, and this pathway requires the IL-4 receptor alpha chain. Selective IL-13 neutralization in murine asthma models, IL-13 administration to T cell-deficient mice, IL-4Rα-deficient mice Science (New York, N.Y.) High 9856949 9856950
1998 IL-13 is required for resistance to the intestinal nematode Trichuris muris; IL-13 knockout mice are susceptible despite being able to mount Th2 responses at later time points, demonstrating a non-redundant role for IL-13 in intestinal helminth immunity distinct from IL-4. IL-13 knockout mice, T. muris infection model, cytokine and antibody isotype analysis Journal of immunology (Baltimore, Md. : 1950) High 9531306
2000 A conserved noncoding element was identified as a coordinate regulator of IL-4, IL-13, and IL-5 gene expression over a 120-kilobase region on chromosome 5q, demonstrated by YAC transgenic mice. Cross-species sequence comparison, YAC transgenic mice, gene expression analysis Science (New York, N.Y.) High 10753117
2001 IL-13 alters mucociliary differentiation of human nasal epithelial cells: it decreases ciliated cell differentiation, increases secretory cell proportion, downregulates ezrin and other cytoskeletal components, impairs apical localization of ezrin, and decreases ciliary beat frequency in a time- and dose-dependent manner; these effects are mediated through the IL-4 receptor alpha subunit (blocked by an IL-4 antagonistic mutant Y124D). Primary human nasal epithelial cell cultures, immunofluorescence, receptor antagonist, time-lapse microscopy of ciliary beat The Journal of clinical investigation High 11748265
2001 IL-13 induces mucin production via a cascade requiring EGFR signaling and neutrophil recruitment; IL-13 induces IL-8-like chemoattractant expression in airway epithelium, recruits neutrophils, and EGFR tyrosine kinase inhibition or neutrophil depletion prevents IL-13-induced goblet cell metaplasia. In vivo intratracheal instillation in mice, EGFR inhibitor, cyclophosphamide-mediated neutrophil depletion, anti-IL-8 blocking antibody American journal of physiology. Lung cellular and molecular physiology High 11133503
2001 IL-13 induces airway hyperreactivity, mucus hypersecretion, eotaxin production, and eosinophilia in the allergic lung through a pathway that requires STAT6 but can operate independently of the IL-4Rα chain, identifying a novel STAT6-dependent component of the IL-13 receptor signaling system. OVA-specific CD4+ T cell transfer to IL-13-deficient, IL-4Rα-deficient, and STAT6-deficient mice with OVA aerosol challenge Journal of immunology (Baltimore, Md. : 1950) High 11466392
2003 IL-13 directly modulates airway smooth muscle (ASM) contractility: it significantly increases carbachol- and KCl-induced maximal force generation in murine tracheal rings and augments cytosolic calcium responses to bradykinin, histamine, and carbachol in cultured human ASM cells, suggesting IL-13 promotes bronchial hyperresponsiveness by enhancing GPCR-associated calcium signaling. Murine tracheal ring contractility assay, calcium fluorimetry in cultured human ASM cells British journal of pharmacology Medium 14597600
2003 IL-13 induces goblet cell metaplasia in human bronchial epithelial cells through MAP kinase (MEK, p38 MAPK) and phosphatidylinositol 3-kinase signaling pathways, independent of EGFR-TK, in a concentration-dependent manner. Air-liquid interface cultures, Alcian blue/MUC5AC staining, kinase inhibitors (PD-98059, U-0126, SB-202190, LY-294002, AG-1478) American journal of physiology. Lung cellular and molecular physiology Medium 12794003
2003 IL-13 suppresses iNOS protein levels in inflammatory macrophages through translational inhibition caused by arginine depletion via arginase induction; although iNOS mRNA remains unaltered, arginase-mediated arginine depletion selectively impairs de novo iNOS protein synthesis and stability, revealing a novel translational regulatory mechanism. Mouse peritoneal macrophage stimulation with IFN-γ/LPS ± IL-13, arginase inhibitors, arginase addition, arginine-free medium, [35S]-methionine incorporation Journal of immunology (Baltimore, Md. : 1950) High 14568929
2005 IL-13 signaling through IL-13Rα2 (formerly considered only a decoy receptor) activates an AP-1 variant containing c-jun and Fra-2, which then activates the TGFB1 promoter; in vivo, IL-13Rα2 silencing reduces TGF-β1 production and collagen deposition in models of colitis and lung fibrosis, establishing IL-13Rα2 as a signaling receptor mediating fibrosis. Macrophage stimulation, AP-1 activation assays, promoter analysis, siRNA knockdown, in vivo colitis and bleomycin lung fibrosis models, collagen quantification Nature medicine High 16327802
2005 The IL-13 R130Q variant (encoded by IL13+2044GA) is significantly more active than WT IL-13 in inducing STAT6 phosphorylation and CD23 expression in monocytes and IgE switching in B cells; it is also neutralized less effectively by the IL-13Rα2 decoy receptor, contributing to enhanced in vivo activity of the variant. Recombinant WT and R130Q IL-13 proteins, STAT6 phosphorylation assay, CD23 expression (flow cytometry), IgE switching assay, IL-13Rα2 neutralization assay on primary human cells The Journal of clinical investigation High 15711639
2005 The IL-13 Gln110 variant (corresponding to R130Q) shows lower affinity for the IL-13Rα2 decoy receptor, causing reduced clearance, and also demonstrates enhanced stability in plasma; asthmatic patients homozygous for this variant have higher serum IL-13 levels, mechanistically linking the SNP to increased IL-13 bioavailability. Recombinant protein binding affinity assays, plasma stability assays, serum IL-13 ELISA in genotyped patients The Journal of allergy and clinical immunology High 12063528
2007 IL-13 treatment of esophageal epithelial cells induces eotaxin-3 production through a transcriptional mechanism dependent on STAT6; IL-13 stimulation recapitulates the EE-specific esophageal transcriptome, and this transcriptome is reversible with glucocorticoid treatment. Primary esophageal epithelial cell cultures, microarray, real-time PCR, luciferase reporter assays with eotaxin-3 promoter fragments and STAT6 mutants The Journal of allergy and clinical immunology High 18073124
2007 IL-33 induces IL-13 (and IL-6) production by mouse mast cells independently of IgE-FcεRI signals via a MyD88-dependent but TRIF-independent pathway; this effect is more potent than IL-1β or IL-18 and does not induce mast cell degranulation. Bone marrow-derived mast cell cultures, cytokine ELISA, MyD88-deficient mice, degranulation assay Journal of leukocyte biology High 17881510
2007 IL-13 secreted by airway epithelial cells after mechanical injury enhances epithelial repair via autocrine induction of HB-EGF (but not EGF), leading to EGFR phosphorylation; neutralization of IL-13 reduces repair, and EGFR inhibition increases IL-13 release, indicating a negative feedback loop between EGFR and IL-13 during repair. Scratch wound assay in AEC monolayers, IL-13 neutralization with sIL-13Rα2.FC, ELISA, EGFR phosphorylation western blot, EGFR kinase inhibitor tyrphostin AG1478 American journal of respiratory cell and molecular biology High 17717322
2007 IL-9 promotes lung eosinophilia and mucus production through an IL-13-dependent mechanism: hematopoietic cells expressing both IL-9R and IL-13 are required for IL-9 effects on lung epithelial cells, establishing IL-13 as a direct downstream mediator of IL-9 on epithelial targets. IL-13 knockout mice crossed with IL-9 transgenic mice, hematopoietic cell transfer experiments with IL-9R-deficient recipients Journal of immunology (Baltimore, Md. : 1950) High 17312173
2007 IL-13 induces CD36 expression in human monocytes through PPARγ activation; this occurs via phospholipase A2-dependent production of endogenous 15-deoxy-Δ12,14-prostaglandin J2 (a PPARγ ligand), which translocates to the nucleus; CD36 and PPARγ are required for IL-13-mediated phagocytosis of P. falciparum-parasitized erythrocytes. PPARγ expression plasmid transfection in RAW264.7, PPARγ conditional null macrophages, PLA2 inhibitors, PGJ2 ELISA, nuclear localization assay, phagocytosis assay European journal of immunology High 17458857
2008 IL-13 signaling through IL-13Rα2 in chronic colitis induces a fibrogenic program comprising TGF-β1 activation, IGF-I and Egr-1 expression, caspase-mediated myofibroblast apoptosis, urokinase plasminogen activator production, and IGF-I/TGF-β1-driven collagen deposition; blockade of IL-13Rα2 or TGF-β1 signaling with siRNA or decoy oligonucleotides abrogates this cascade. TNBS chronic colitis mouse model, siRNA targeting IL-13Rα2 and TGF-β1 signaling components, ELISA, Western blot, collagen measurement Gastroenterology High 18938165
2008 Crystal structures of the complete type I (IL-4Rα/γc/IL-4) and type II (IL-4Rα/IL-13Rα1/IL-4 and IL-4Rα/IL-13Rα1/IL-13) ternary signaling complexes reveal that IL-13 engages IL-13Rα1 via an unusual top-mounted Ig-like domain in a novel mode of cytokine engagement; the two type II complexes use substantially different recognition chemistries and have a reversed assembly sequence compared to type I; type II receptor signals with different potencies for IL-4 versus IL-13. X-ray crystallography of complete ternary receptor complexes, functional signaling assays Cell High 18243101
2008 MMP-8 cleaves IL-13Rα2 in vitro and contributes to solubilization of IL-13Rα2 in vivo; MMP-8-deficient mice display increased airway hyperresponsiveness and decreased soluble IL-13Rα2 in bronchoalveolar lavage after allergen challenge; the solubilized IL-13Rα2 retains IL-13 binding activity. In vitro acellular cleavage assays with GST-fusion proteins, stable-transfected cell surface expression assay, MMP-8-deficient mice, allergen challenge model, BAL fluid analysis The Journal of allergy and clinical immunology High 18694590
2008 IL-13 attenuates vascular tube (capillary-like) formation and endothelial cell migration via JAK2 activation followed by STAT6 activation; depletion of JAK2 and STAT6 by RNA interference abolishes the anti-angiogenic effect of IL-13. In vitro tube formation assay in human coronary artery endothelial cells, siRNA knockdown of JAK2 and STAT6, migration assay Circulation journal Medium 18296848
2010 IL-13 mediates collagen deposition via STAT6 and epigenetic repression of microRNA-135b in dermal fibroblasts; STAT6 knockdown blocks IL-13-induced collagen1A1 expression; miR-135b overexpression reduces IL-13-induced collagen induction; scleroderma fibroblasts have constitutively lower miR-135b due to methylation-dependent repression involving MeCP2. siRNA knockdown of STAT6, small molecule STAT6 inhibitor, miR-135b transfection, qRT-PCR, methylation analysis in patient-derived fibroblasts Scientific reports Medium 27113293
2010 IL-13 promotes beige fat biogenesis through IL-4/IL-13 signaling in alternatively activated macrophages; macrophages recruited to cold-stressed subcutaneous white adipose tissue undergo alternative activation to express tyrosine hydroxylase and produce catecholamines required for browning; genetic loss of IL-4/IL-13 signaling impairs cold-induced beige fat development. Genetic mouse models deficient in eosinophils or IL-4/IL-13 signaling, cold exposure experiments, macrophage tyrosine hydroxylase immunostaining, catecholamine measurements Cell High 24906148
2010 MiR-155 directly targets IL-13Rα1 mRNA in human macrophages, reducing IL-13Rα1 protein levels and diminishing STAT6 phosphorylation in response to IL-13, thereby modulating expression of M2 marker genes (SOCS1, DC-SIGN, CCL18, CD23, SERPINE). Bioinformatics prediction, luciferase reporter assay, western blot, STAT6 phosphorylation, gene expression analysis in primary human macrophages with miR-155 overexpression/inhibition The Journal of biological chemistry High 21097505
2010 IL-13 downregulates desmoglein-1 (DSG1) in esophageal epithelial cells, impairing barrier function; DSG1 silencing induces transcriptional changes overlapping the EoE transcriptome, including induction of periostin (POSTN), linking IL-13-driven DSG1 loss to esophageal barrier dysfunction and pro-inflammatory mediator production. IL-13 stimulation of primary esophageal epithelial cells, DSG1 siRNA knockdown, transepithelial resistance measurement, transcriptomic analysis, patient biopsy validation Mucosal immunology High 24220297
2011 Let-7 microRNAs directly regulate IL-13 expression; induced IL-13 levels in T cells are inversely related to let-7 levels, and intranasal delivery of let-7 mimic in allergic mice decreases IL-13 levels and resolves airway inflammation, airway hyperresponsiveness, mucus metaplasia, and subepithelial fibrosis. Bioinformatics, in vitro transfection in A549 cells and primary T cells, in vivo let-7 mimic intranasal delivery in murine allergic inflammation model The Journal of allergy and clinical immunology Medium 21616524
2013 Chitinase 3-like 1 (Chi3l1) binds to IL-13Rα2 and is found in a multimeric complex with IL-13Rα2 and IL-13; Chi3l1 activates MAPK, AKT, and Wnt/β-catenin signaling via IL-13Rα2-dependent mechanisms to regulate apoptosis, pyroptosis, inflammasome activation, antibacterial responses, and TGF-β1 production. Co-immunoprecipitation, pulldown assays, IL-13Rα2-deficient cells, pharmacological pathway inhibitors, functional readouts Cell reports High 23972995
2016 IL-13 promotes intestinal SIgA secretion through a pathway involving intestinal microbiota and IL-13; injection of an IL-13 antibody during glutamine supplementation reduces J-chain expression in the mouse ileum, and disrupting the intestinal microbiota abrogates glutamine's effect on SIgA, with IL-13 acting as a mediator in the T cell-dependent SIgA induction pathway. Mouse model with glutamine supplementation, IL-13 neutralizing antibody injection, IL-13 ELISA, J-chain expression, germ-free/antibiotic-treated mice Molecular nutrition & food research Low 27005687
2017 IL-33 drives a signaling cascade to IL-13 that is required for spasmolytic polypeptide-expressing metaplasia (SPEM) induction in the stomach after parietal cell loss; IL-33 KO and ST2 KO mice do not develop metaplasia in response to L635, while IL-13 KO mice also fail to develop SPEM, and exogenous IL-13 restores metaplasia in ST2 KO mice. IL-33, ST2, and IL-13 knockout mice, L635-induced parietal cell loss model, exogenous IL-13 rescue, macrophage RNA sequencing Gut High 28196875
2017 IL-4 or IL-13 together with apoptotic cells (but not alone) is required to induce the tissue repair program in macrophages; genetic ablation of apoptotic cell sensors impairs macrophage proliferation and anti-inflammatory/repair gene induction in the lungs after helminth infection or colitis, while recognition of apoptotic cells is dispensable for cytokine-dependent induction of pattern recognition receptor or chemotaxis genes. Genetic ablation of apoptotic cell sensors, helminth infection model, colitis model, macrophage gene expression analysis Science (New York, N.Y.) High 28495875
2017 Autophagy is required for IL-13-mediated apical localization of DUOX1 and subsequent intracellular superoxide production in airway epithelial cells; depletion of autophagy regulator ATG5 reduces superoxide without diminishing total DUOX1 levels, but diminishes apical DUOX1 localization, while DUOX1 siRNA attenuates IL-13-induced superoxide without affecting autophagy. Primary human tracheobronchial epithelial cells, OVA mouse model, ATG5 siRNA, DUOX1 siRNA, EPR spectroscopy for superoxide, LC3BII western blot, immunostaining Redox biology Medium 28982074
2019 IL-13 secreted by ILC2s promotes Lgr5+ intestinal stem cell self-renewal through a circuit involving circPan3 and IL-13Rα1; circPan3 binds IL-13Rα1 mRNA to increase its stability, enabling ISC expression of IL-13Rα1; IL-13 signaling through IL-13Rα1 activates Foxp1 expression, which associates with β-catenin to promote its nuclear translocation and activate Wnt/β-catenin pathway in ISCs. circPan3 deletion in Lgr5+ ISCs, IL-13Rα1 mRNA stability assay (RNA-protein interaction), Foxp3Cre mouse model, β-catenin localization, organoid/stem cell assays Nature immunology High 30643264
2019 Foxp3+ Tregs secrete IL-13 in response to IL-33 stimulation, and Treg-derived IL-13 is required to prevent mortality after acute lung injury by controlling local levels of G-CSF, IL-6, and MCP-1 and inhibiting accumulation of Ly6Chi monocytes; this was demonstrated using Foxp3Cre × Il4/Il13fl/fl mice. Foxp3Cre × Il4/Il13fl/fl conditional knockout mice, acute lung injury model, BAL cytokine analysis, monocyte flow cytometry, IL-33 stimulation of human and mouse Tregs JCI insight High 30779711
2019 Akt1 regulates IL-13 production by macrophages; Akt1-deficient macrophages produce less IL-13 compared to Akt1+/+ macrophages in response to IL-33 stimulation; Akt1-deficient mice have reduced IL-13 levels after bleomycin treatment and are protected from pulmonary fibrosis. Akt1 knockout mice, bleomycin fibrosis model, bone marrow-derived macrophage stimulation with IL-33, IL-13 ELISA, collagen/ECM quantification Innate immunity Medium 31299858
2021 Eosinophil-derived IL-13 produced via ST2 (IL-33 receptor) signaling is required for hepatoprotection against ischemia-reperfusion injury; adoptive transfer of bone marrow-derived eosinophils reduces hepatic injury, and this protection requires ST2-dependent IL-13 production by eosinophils, established through genetic and adoptive transfer approaches. Two genetic mouse models of eosinophil deficiency, antibody-mediated eosinophil depletion, adoptive transfer of eosinophils, ST2-deficient eosinophils, liver IRI model, liver injury biochemical/histological assessment Science translational medicine High 33536281

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature 3725 23128233
1998 Interleukin-13: central mediator of allergic asthma. Science (New York, N.Y.) 2100 9856949
2010 A large-scale, consortium-based genomewide association study of asthma. The New England journal of medicine 1582 20860503
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1998 Requirement for IL-13 independently of IL-4 in experimental asthma. Science (New York, N.Y.) 1477 9856950
2009 Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways. Nature genetics 1160 19169254
1993 Interleukin-13 is a new human lymphokine regulating inflammatory and immune responses. Nature 869 8096327
2001 IL-13 effector functions. Annual review of immunology 763 12615888
2005 IL-13 signaling through the IL-13alpha2 receptor is involved in induction of TGF-beta1 production and fibrosis. Nature medicine 748 16327802
2014 Eosinophils and type 2 cytokine signaling in macrophages orchestrate development of functional beige fat. Cell 717 24906148
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2000 Identification of a coordinate regulator of interleukins 4, 13, and 5 by cross-species sequence comparisons. Science (New York, N.Y.) 626 10753117
2004 Nonclassical CD1d-restricted NK T cells that produce IL-13 characterize an atypical Th2 response in ulcerative colitis. The Journal of clinical investigation 609 15146247
1993 Interleukin 13, a T-cell-derived cytokine that regulates human monocyte and B-cell function. Proceedings of the National Academy of Sciences of the United States of America 531 8097324
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