Affinage

IL25

Interleukin-25 · UniProt Q9H293

Length
177 aa
Mass
20.3 kDa
Annotated
2026-06-10
100 papers in source corpus 37 papers cited in narrative 37 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

IL-25 (IL-17E) is an epithelial- and tuft-cell-derived cytokine of the IL-17 family that serves as a master initiator of type 2 immunity, signaling through the receptor IL-17RB (IL-17BR/EVI27) to drive IL-4, IL-5, and IL-13 production, eosinophilia, IgE responses, and barrier-tissue inflammation (PMID:11058597, PMID:11754819, PMID:26675736). Receptor engagement activates NF-κB via constitutively associated TRAF6 and parallel ERK/JNK/p38 MAPK cascades to induce proinflammatory chemokines and Th2-skewing genes (PMID:11058597, PMID:16393988); ACT1 recruitment to IL-17RB requires TRAF4, which directs SMURF2-mediated degradation of the inhibitor DAZAP2, while a distinct set of IL-17RB tyrosines supports a parallel Act1-independent STAT5 branch essential for Th2 polarization (PMID:25681341, PMID:25821217). IL-25 acts on a range of innate effectors—ILC2s, multipotent MPPtype2 progenitors, Th2 and Th9 cells—to amplify type 2 cytokines, with ILC2-derived IL-13 sufficient to drive airway hyperresponsiveness, fibrosis, and epithelial remodeling (PMID:20200520, PMID:20154671, PMID:24344271, PMID:23960191, PMID:26675736). In the intestine, tuft-cell-derived IL-25 establishes a feed-forward circuit with ILC2-derived IL-13 that drives tuft and goblet cell differentiation and anti-helminth immunity (PMID:26675736). Beyond type 2 immunity, IL-25 restrains Th17 responses by inducing IL-13 that suppresses dendritic-cell IL-23/IL-1β/IL-6, defining an IL-25–IL-23–IL-17 axis shaped by commensal microbiota (PMID:17200411, PMID:18762568); it also promotes M2 macrophage polarization, keratinocyte proliferation and motility, endothelial angiogenesis via VEGF, and innate skin inflammation through macrophage p38-dependent neutrophil recruitment (PMID:21205894, PMID:35008429, PMID:30738055, PMID:31958433). Epithelial IL-25 production is itself gated by mTOR-suppressed autophagy and modulated by IL-22 and protease allergens (PMID:20514301, PMID:21794904, PMID:33077617). A recent finding extends IL-25 to neuromodulation, where cortical-neuron-derived IL-17E acts on IL-17RB-expressing cortical neurons to regulate social behavior (PMID:40199322).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 2001 High

    Establishing that IL-25 is a functional ligand for IL-17RB that triggers NF-κB and chemokine output defined its molecular identity as a signaling cytokine.

    Evidence Receptor-ligand binding, NF-κB reporter, and IL-8 production assays in vitro

    PMID:11058597

    Open questions at the time
    • Did not define the second receptor chain or the downstream adaptor
    • Physiological cellular source not addressed
  2. 2001 High

    In vivo infusion and transgenic overexpression showed IL-25 is sufficient to drive a systemic Th2 cytokine cascade, IgE responses, and eosinophilia, framing it as an initiator of type 2 immunity.

    Evidence Cytokine infusion and transgenic mouse models with serum Ig, cytokine, histology, and flow readouts

    PMID:11714825 PMID:11754819 PMID:12239140

    Open questions at the time
    • Lineage-negative responding cell identity left undefined
    • Did not resolve direct versus indirect cytokine induction
  3. 2002 High

    Genetic epistasis placed IL-5 and IL-13 (not IL-4 or T cells) as the obligate downstream effectors of IL-25-induced eosinophilia, narrowing the effector arm.

    Evidence Adenoviral IL-25 delivery in cytokine- and T-cell-deficient mice with BAL and flow analysis

    PMID:12077275

    Open questions at the time
    • Identity of the gamma-common-dependent innate responder cell not resolved
    • Did not address receptor signaling mechanism
  4. 2006 High

    Identifying TRAF6 as the constitutively associated adaptor required for IL-25R-driven NF-κB and demonstrating MAPK activation defined the proximal signaling machinery.

    Evidence Receptor cross-linking, dominant-negative and TRAF6-deficient MEFs, reciprocal Co-IP, gene expression

    PMID:16393988

    Open questions at the time
    • Role of ACT1 and receptor tyrosines not yet defined
    • Did not address non-NF-κB branches
  5. 2006 Medium

    Demonstrating that lung fibroblasts and airway smooth muscle constitutively express IL-17BR and respond to IL-25 with chemokine and ECM gene induction, with receptor levels tuned by TNF-α and IFN-γ, extended IL-25 action to structural cells.

    Evidence Primary fibroblast and airway smooth muscle cultures, pharmacological pathway inhibitors, PCR/ELISA

    PMID:16428271 PMID:16522458

    Open questions at the time
    • Single-lab findings
    • In vivo relevance of ECM induction not established
  6. 2007 High

    STAT6- and CD4-dependent epistasis plus discovery that IL-25 suppresses Th17 responses via IL-13-mediated inhibition of dendritic-cell IL-23 revealed IL-25 as both a type 2 amplifier and a Th17 brake.

    Evidence STAT6 KO, CD4 depletion, transgenic and IL-25 KO mice in airway and EAE models with DC stimulation assays

    PMID:16950278 PMID:17177681 PMID:17200411 PMID:17719653

    Open questions at the time
    • Receptor-level basis of STAT6 engagement not defined
    • Cell-type source of protective IL-25 in EAE unresolved
  7. 2008 High

    Commensal-dependent suppression of epithelial IL-25 in the gut defined an IL-25–IL-23–IL-17 regulatory axis tuned by microbiota, situating IL-25 in intestinal immune homeostasis.

    Evidence Germ-free mouse model with epithelial sorting, cytokine quantification, T-cell flow cytometry

    PMID:18762568

    Open questions at the time
    • Molecular sensor linking microbiota to IL-25 repression unknown
    • Macrophage-IL-23 step not mechanistically dissected
  8. 2010 High

    Discovery that IL-25 expands MPPtype2 progenitors and couples to IL-17RB on Th9 cells to drive IL-9 broadened the cellular targets of IL-25 beyond classical Th2 cells.

    Evidence Flow cytometry, adoptive transfer into Il25-/- mice, retroviral/transgenic IL-17RB overexpression, helminth and airway models

    PMID:20154671 PMID:20200520

    Open questions at the time
    • Relationship between MPPtype2 and ILC2 not yet resolved
    • Signaling basis of IL-9 induction unaddressed
  9. 2010 Medium

    Identifying protease-allergen activation of ERK/p38 as the trigger for epithelial IL-25 induction connected environmental sensing to IL-25 output.

    Evidence Lung epithelial cell stimulation with protease-inactivation controls and MAPK inhibitors plus in vivo BAL

    PMID:20514301

    Open questions at the time
    • Protease receptor/sensor not identified
    • Single-lab finding
  10. 2013 High

    Demonstrating that IL-25-activated ILC2-derived IL-13 is sufficient to drive fibrosis independent of T cells, and that IL-25 preferentially drives MPPtype2 over ILC2 responses, refined the innate effector hierarchy.

    Evidence IL-25 administration in Rag-/- and RORα-deficient mice, genome-wide profiling, adoptive transfer after ILC2 depletion

    PMID:23960191 PMID:24344271

    Open questions at the time
    • Determinants of ILC2 versus MPPtype2 preference unclear
    • Receptor signaling distinguishing the two not defined
  11. 2014 High

    Receptor blockade and IL-25 neutralization in rhinovirus models established IL-25 as a driver of viral exacerbation of type 2 airway inflammation, including an age-dependent ILC2 response.

    Evidence Murine RV infection with IL-17RB blockade or anti-IL-25, cell recruitment and ILC2 flow cytometry

    PMID:24910174 PMID:25273095

    Open questions at the time
    • Mechanism by which RV induces epithelial IL-25 not fully defined
    • Human translation not directly tested in vivo
  12. 2015 High

    Defining the tuft-cell origin of IL-25 and the tuft–ILC2–IL-13 feed-forward circuit established the cellular architecture of intestinal type 2 epithelial remodeling.

    Evidence Tuft-cell IL-25 expression, helminth infection, IL-13 neutralization, epithelial progenitor differentiation assays

    PMID:26675736

    Open questions at the time
    • Tuft cell sensing input upstream of IL-25 not defined here
    • Receptor signaling in ILC2 not dissected
  13. 2015 High

    Identifying the TRAF4-SMURF2-DAZAP2 axis enabling ACT1 recruitment and a parallel Act1-independent STAT5 branch through specific IL-17RB tyrosines resolved the bifurcated proximal signaling of IL-25.

    Evidence Traf4-/- and STAT5 conditional KO mice, Co-IP of TRAF4/SMURF2/DAZAP2, IL-17RB tyrosine mutagenesis, Th2 polarization assays

    PMID:25681341 PMID:25821217

    Open questions at the time
    • Structural basis of tyrosine-specific STAT5 recruitment unresolved
    • Cell-type specificity of the two branches not fully mapped
  14. 2016 Medium

    Demonstrating receptor-mediated clathrin-dependent uptake of IL-25 by M2 macrophages, and selective caspase-driven apoptosis in IL-17RB-high breast cancer cells, expanded IL-25 biology to non-canonical receptor responses and tumor contexts.

    Evidence Psoriatic biopsy IHC, macrophage polarization and endocytosis assays, 3D breast cancer cultures with caspase assays

    PMID:21490275 PMID:27329229

    Open questions at the time
    • Signaling downstream of endocytosed IL-25 not defined
    • Single-lab findings
  15. 2017 Medium

    Linking IL-25-driven M2 polarization to AMPK activation and PINK1-dependent mitophagy provided a metabolic mechanism for macrophage reprogramming.

    Evidence THP-1 monocytes with mitochondrial complex assays, AMPK/mitophagy Western blots, PINK1 knockdown, CCL-22 ELISA

    PMID:35008429

    Open questions at the time
    • Receptor-to-AMPK coupling not defined
    • Single cell-line system
  16. 2019 High

    Genetic and neutralization studies established IL-25 as a driver of innate skin inflammation, keratinocyte proliferation/motility, angiogenesis, and Th17-mediated contact hypersensitivity via diverse effector mechanisms.

    Evidence Il17e-/- mice, neutralization in imiquimod/tape-stripping and CHS models, macrophage-neutrophil co-culture with p38 inhibition, HUVEC angiogenesis, keratinocyte cultures

    PMID:21205894 PMID:29522843 PMID:30738055 PMID:31958433

    Open questions at the time
    • Receptor signaling underlying keratinocyte and endothelial responses not fully mapped
    • Context determining type 2 versus type 17 output unclear
  17. 2020 High

    Defining keratinocyte-derived IL-25 as an ILC2-activating trigger of allergic skin inflammation, and showing mTOR-suppressed autophagy gates epithelial IL-25 production, connected barrier IL-25 output to upstream regulation and downstream type 2 pathology.

    Evidence Cell-type-specific IL-25/IL-17RB conditional KO and IL-13 reporter mice; airway MTOR-KD and Lc3b-/- mice with IL-25 blockade

    PMID:32179159 PMID:33077617

    Open questions at the time
    • Signal linking autophagy to IL-25 transcription/secretion not defined
    • Acute versus chronic IL-13 source switch mechanism unresolved
  18. 2021 High

    Showing that tuft-cell cysteinyl leukotrienes and IL-25 synergistically activate ILC2s and dendritic cells revealed combinatorial epithelial signals shaping type 2 lung inflammation.

    Evidence Tuft-cell-specific Ltc4s deletion, IL-25 blockade, CysLT receptor pharmacology, LTC4 plus subthreshold IL-25 co-administration

    PMID:34932383

    Open questions at the time
    • Molecular basis of LTC4/IL-25 synergy at the ILC2 level not defined
  19. 2025 Medium

    Identifying cortical-neuron-derived IL-25 acting on IL-17RB-expressing cortical neurons to regulate social behavior extended IL-25 into neuromodulation beyond immunity.

    Evidence Brain-wide receptor mapping, genetic IL-17RB deletion, social behavior assays

    PMID:40199322

    Open questions at the time
    • Neuronal signaling pathway downstream of IL-17RB not defined
    • Single-study novel function awaiting independent confirmation

Open questions

Synthesis pass · forward-looking unresolved questions
  • How distinct IL-17RB tyrosine-coupled branches (TRAF6/ACT1 NF-κB versus STAT5) are differentially deployed across cell types, and how upstream sensors gate IL-25 release in epithelial, neuronal, and tumor contexts, remain open.
  • No structural model of the ligand-receptor-adaptor assembly
  • Cell-type logic of branch selection unresolved
  • Sensor coupling autophagy/protease/microbiota to IL-25 transcription incompletely defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 3 GO:0060089 molecular transducer activity 3
Localization
GO:0005576 extracellular region 3
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 4
Partners
ACT1DAZAP2IL17RAIL17RBSMURF2STAT5TRAF4TRAF6

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 IL-25 (IL-17E) was identified as a ligand for the receptor EVI27/IL-17Rh1 (IL-17BR/IL-17RB). Binding induces NF-κB activation and stimulates production of the proinflammatory chemokine IL-8. Receptor-ligand binding assay, NF-κB reporter assay, IL-8 production assay in vitro The Journal of biological chemistry High 11058597
2001 Infusion of IL-25 into mice induced IL-4, IL-5, and IL-13 gene expression and Th2-like responses (elevated serum IgE, IgG1, IgA, blood eosinophilia, lung and gut pathology). IL-25 induced Th2-type cytokine production by MHC class II-high, CD11c-dull, lineage-negative accessory cells. In vivo cytokine infusion in mice, gene expression analysis, serum immunoglobulin measurement, histology, flow cytometry of responding cell populations Immunity High 11754819
2001 Transgenic overexpression of murine IL-17E induces a Th2-biased immune response characterized by eosinophilia, elevated serum IL-13 and IL-5, increased IgE/IgG1, and multi-organ inflammatory pathology. IL-17E also induces G-CSF production in vitro and neutrophilia in vivo. Transgenic mouse model, serum cytokine and immunoglobulin measurement, histology, in vitro G-CSF assay Journal of immunology High 11714825
2002 Intranasal IL-25 induces IL-4, IL-5, IL-13, and eotaxin mRNA in the lung and marked eosinophilia. IL-25-induced eosinophilia requires IL-5 and IL-13 but not IL-4 or T cells, and requires a gamma-common cytokine receptor-dependent cell population that is B220+, Thy-1+/-, NK1.1-, Ly-6G-, CD4-, CD3-, c-kit-negative. Adenoviral in vivo delivery, cytokine-deficient and T-cell-deficient mouse models, flow cytometry of responding cell populations, bronchoalveolar lavage analysis Journal of immunology High 12077275
2002 Transgenic overexpression of human IL-17E in mice driven by ApoE hepatic promoter causes eosinophilia, B-lymphocyte hyperplasia, elevated serum IL-2, IL-4, IL-5, G-CSF, eotaxin, IFN-γ, and increased IgM, IgG, IgE. In situ hybridization revealed upregulation of the IL-17E receptor IL-17Rh1 (IL-17BR/Evi27) in transgenic tissues. Transgenic mouse model (ApoE promoter), flow cytometry, serum cytokine/immunoglobulin ELISA, in situ hybridization Blood High 12239140
2006 IL-25R (IL-17RB) cross-linking activates NF-κB and MAPK pathways (ERK, JNK, p38). NF-κB activation is mediated specifically by TRAF6 (not TRAF2): dominant-negative TRAF6 blocked IL-25R-mediated NF-κB activation, and NF-κB activation was absent in TRAF6-deficient fibroblasts. TRAF6 co-immunoprecipitates with IL-25R even in the absence of ligand. TRAF6 is required for IL-25R-mediated gene expression of IL-6, TGF-β, G-CSF, and TARC. Receptor cross-linking assay, dominant-negative transfection, TRAF6-deficient murine embryonic fibroblasts, co-immunoprecipitation, NF-κB reporter assay, gene expression analysis Journal of immunology High 16393988
2006 IL-17E (IL-25) upregulates CCL5, CCL11 (eotaxin), GM-CSF, and CXCL8 mRNA in human primary lung fibroblasts, which constitutively express IL-17BR. IL-17E and TNF-α synergistically induce GM-CSF and CXCL8 production and secretion. TGF-β1 modulates IL-17E-induced responses. IL-17BR mRNA is upregulated by TNF-α and downregulated by TGF-β1. Primary fibroblast culture, immunofluorescence, Western blot, real-time PCR, ELISA, cytokine stimulation The Journal of allergy and clinical immunology Medium 16522458
2006 TNF-α upregulates IL-17BR expression in airway smooth muscle cells primarily through NF-κB (blocked by IKK2 inhibitor AS-602868). IFN-γ downregulates IL-17BR via the ERK pathway (blocked by MEK inhibitor U0126). IL-17E stimulation of airway smooth muscle cells increases expression of ECM components procollagen-αI and lumican mRNA. In vitro airway smooth muscle cell culture, pharmacological inhibitors (NF-κB, MEK/ERK), real-time PCR, Western blot, immunohistochemistry of asthmatic biopsies American journal of physiology. Lung cellular and molecular physiology Medium 16428271
2006 IL-25-induced airway hyperresponsiveness (AHR) and eosinophilic inflammation are dependent on IL-13, IL-4Rα (IL-4 receptor alpha), and STAT6 signaling, as shown by significantly reduced AHR and mucus production in IL-13−/−, IL-4Rα−/−, and STAT6−/− mice. IL-4 and IL-5/eotaxin1 deficiency also reduced AHR but not mucus hypersecretion. IL-25 can directly act on naïve T cells to promote Th2 responses. Intratracheal IL-25 instillation in cytokine-deficient mouse strains, plethysmography, histology, BAL analysis Clinical and experimental allergy High 17177681
2007 IL-25-deficient mice are highly susceptible to experimental autoimmune encephalomyelitis (EAE), associated with increased IL-23 in the periphery and increased IL-17-, IFN-γ-, and TNF-producing T cells. IL-25 suppresses Th17 responses by inducing IL-13, which directly inhibits IL-23, IL-1β, and IL-6 expression in activated dendritic cells. IL-25 knockout mice, EAE model, cytokine neutralization (anti-IL-17, anti-IFN-γ), IL-25 treatment in relapsing-remitting and chronic EAE models, dendritic cell stimulation assays The Journal of experimental medicine High 17200411
2007 IL-25 enhances antigen-induced Th2 cytokine production, eosinophil recruitment, and goblet cell hyperplasia in allergic airway inflammation through a Th2 cell-dependent pathway requiring CD4+ T cells and STAT6. Transgenic enforced expression of IL-25 in lung (Clara cell promoter) alone is insufficient to induce inflammation but potentiates allergen-driven responses. IL-25 transgenic mice (CC10 promoter), CD4+ T cell depletion, STAT6-deficient mice, OVA sensitization model, BAL analysis, histology The Journal of allergy and clinical immunology High 16950278
2007 IL-25 synergistically induces release of Th2 cytokines (IL-4, IL-5, IL-10), IL-6, and chemokines (CXCL9, CXCL10, CCL5) from anti-CD3/CD28 costimulated human memory Th cells. Costimulation upregulates IL-25R surface expression on Th cells. The cytokine release is differentially regulated by JNK, p38 MAPK, and NF-κB pathways. Human T cell culture with anti-CD3/CD28 costimulation and IL-25, bead-based multiplex cytokine array, flow cytometry for receptor expression, EMSA for NF-κB, Western blot for MAPK, pharmacological inhibitors Immunology letters Medium 17719653
2008 Commensal bacteria suppress intestinal IL-25 expression by intestinal epithelial cells. In germ-free mice, elevated Th17 cell frequency in the large intestine is associated with reduced IL-25. Commensal-dependent IL-25 limits expansion of Th17 cells by inhibiting macrophage-derived IL-23, defining an IL-25–IL-23–IL-17 axis. Germ-free mouse model, microbiota colonization, epithelial cell sorting, cytokine quantification, T cell frequency by flow cytometry The Journal of experimental medicine High 18762568
2009 Allergen-induced stem cell factor (SCF) promotes IL-25 (IL-17E) production from c-kit+ eosinophils in the lung; bone marrow-derived mast cells did not produce IL-25 in response to SCF. The IL-25R (IL-17RB) was expressed on a CD11b+GR1+Ly6C+/- c-kit- myeloid cell population that is the major source of Th2 cytokines (IL-4) in the lung during chronic allergen challenge. SCF neutralization in allergen-challenged mice, sorted cell populations for cytokine expression, 4get IL-4 reporter mice, flow cytometry, bone marrow-derived mast cell assay Journal of immunology Medium 19828636
2010 IL-25 promotes accumulation of a lineage-negative multipotent progenitor (MPPtype2) cell population (Sca-1+, c-Kitint) in gut-associated lymphoid tissue. MPPtype2 cells exhibit multipotent capacity giving rise to monocyte/macrophage and granulocyte lineages in vitro and in vivo. Adoptive transfer of MPPtype2 cells promotes Th2 cytokine responses and confers protective immunity to helminth infection in IL-25-deficient mice. Flow cytometry, in vitro and in vivo differentiation assays, adoptive transfer into Il25−/− mice, helminth infection model Nature High 20200520
2010 IL-25 signals through IL-17RB expressed on in-vitro-generated IL-9-expressing T cells (Th9 cells) to enhance IL-9 expression. Transgenic or retroviral overexpression of IL-17RB in T cells results in IL-25-induced IL-9 production independently of IL-4. In vivo, the IL-25–IL-17RB pathway regulates IL-9 expression in allergic airway inflammation. In vitro Th9 cell generation, retroviral/transgenic overexpression of IL-17RB, IL-9 cytokine measurement, allergic airway inflammation mouse model Nature immunology High 20154671
2010 Protease allergens (papain, Der P1) induce IL-25 and TSLP gene expression in mouse lung epithelial cells via protease activity-dependent activation of ERK and p38 MAPK pathways, but not NF-κB or PI-3 kinase pathways. Deactivation of protease activity abolishes IL-25 induction. Mouse lung epithelial cell (MLE12) stimulation, protease inactivation controls, pharmacological MAPK inhibitors, real-time PCR, in vivo BAL cytokine measurement Journal of Korean medical science Medium 20514301
2011 IL-25 enhances survival of human eosinophils and upregulates ICAM-1 surface expression while suppressing ICAM-3 and L-selectin, increasing eosinophil adhesion to fibronectin. These effects are mediated through p38 MAPK (for L-selectin regulation), JNK (for ICAM-1), and NF-κB/proteasome (for ICAM-3) pathways. Human eosinophil culture, flow cytometry for adhesion molecules, fibronectin adhesion assay, pharmacological inhibitors (SB203580, SP600125, MG-132), RT-PCR Allergy Medium 16792588
2011 IL-25 activates caspase-mediated apoptosis in IL-25R (IL-17RB)-expressing breast cancer cells through differential receptor expression; nonmalignant mammary epithelial cells with low IL-17RB expression are spared. IL-17RB is expressed at high levels in tumors from patients with poor prognosis but low in nonmalignant breast tissue. In vitro 3D laminin-rich gel culture, secreted factor screen, caspase activity assays, tumor tissue expression analysis, selective cytotoxicity assays Science translational medicine Medium 21490275
2011 IL-25 stimulates angiogenesis in vitro by increasing HUVEC proliferation and microvessel formation in a concentration-dependent manner. HUVECs constitutively express IL-25R (upregulated by TNF-α). IL-25 increases VEGF and VEGF receptor expression. IL-25-induced angiogenesis is blocked by VEGF neutralization, PI3K inhibitor LY294002, and MEK1/2 inhibitor U0126. In vitro angiogenesis assay (HUVEC), WST-8 proliferation assay, real-time PCR for IL-25R and VEGF, pharmacological inhibitors (LY294002, U0126), immunohistochemistry of asthmatic biopsies Proceedings of the National Academy of Sciences Medium 21205894
2011 IL-22 inhibits IL-13-mediated enhancement of IL-25 expression in lung epithelial cells (MLE-15). Anti-IL-22 antibody in vivo enhanced allergen-induced IL-25 production in airways; anti-IL-25 antibody reversed the enhancing effect of IL-22 blockade on eosinophil recruitment. This places IL-22 upstream of IL-25 in a regulatory axis. Anti-IL-22 neutralization in vivo, intranasal recombinant IL-22 administration, in vitro lung epithelial cell stimulation with IL-22 and IL-13, cytokine measurement by PCR and ELISA The Journal of allergy and clinical immunology Medium 21794904
2013 IL-25 induces pulmonary fibrosis via IL-13 release from ILC2s driving collagen deposition in the lungs. ILC2-derived IL-13 is sufficient to drive fibrosis, independently of T-cell-mediated adaptive immunity. Murine IL-25 administration model, ILC2 characterization, collagen deposition histology, Rag−/− and RORα-deficient mice, cytokine neutralization Proceedings of the National Academy of Sciences High 24344271
2013 IL-25 predominantly promotes MPPtype2 cell responses rather than ILC2 responses at multiple tissue sites. MPPtype2 cells are distinguished from ILC2 by differential transcription factor requirements, distinct genome-wide transcriptional profile, lack of T1/ST2 and IL-7Rα expression, and multipotent functional potential. IL-25-induced MPPtype2 cells promote Th2 cytokine-associated inflammation after ILC2 depletion. Comparative in vivo IL-25 vs IL-33 administration, flow cytometry, genome-wide transcriptional profiling, adoptive transfer after ILC2 depletion, transcription factor-deficient mice The Journal of experimental medicine High 23960191
2014 IL-25 receptor (IL-17RB) blockade in mice reduces rhinovirus (RV)-induced exacerbation-specific responses including type 2 cytokine expression, mucus production, and recruitment of eosinophils, neutrophils, basophils, and T and non-T type 2 cells. RV infection induces IL-25 expression in mouse airways and augments allergen-induced IL-25, positioning IL-25 as a key mediator of RV-induced exacerbation of pulmonary inflammation. Murine RV infection model, IL-25R neutralizing antibody blockade, cytokine gene expression, cell recruitment quantification Science translational medicine High 25273095
2014 Anti-IL-25 neutralizing antibody treatment in neonatal rhinovirus-infected mice attenuates ILC2 expansion, mucous hypersecretion, and airways hyperresponsiveness, establishing IL-25 as the driver of an age-dependent, ILC2-mediated type 2 response to early-life viral infection. Neonatal mouse RV infection model, anti-IL-25 neutralization, flow cytometry for ILC2, histology for mucus, methacholine responsiveness The Journal of allergy and clinical immunology Medium 24910174
2015 Intestinal tuft cells constitutively express IL-25 to sustain ILC2 homeostasis in the resting lamina propria. After helminth infection, tuft-cell-derived IL-25 activates ILC2s to secrete IL-13, which acts on epithelial crypt progenitors to promote differentiation of tuft and goblet cells, forming a response circuit mediating epithelial remodelling. Tuft-cell-specific IL-25 expression analysis, helminth infection model, ILC2 characterization, IL-13 neutralization, intestinal epithelial progenitor differentiation assays, lineage-tracing/flow cytometry Nature High 26675736
2015 IL-25 receptor signaling requires TRAF4, which recruits E3-ligase SMURF2 to degrade the inhibitory molecule DAZAP2, enabling ACT1 interaction with IL-17RB. TRAF4 is required for the ACT1/IL-25R interaction; Traf4−/− mice show blunted IL-25-induced airway eosinophilia and Th2 cytokine production. A specific tyrosine residue within IL-25R is required for DAZAP2-mediated inhibition relief. Traf4−/− mouse model, in vitro knockdown of Dazap2, co-immunoprecipitation (TRAF4/SMURF2/DAZAP2), in vivo IL-25 challenge, cytokine and eosinophil measurement, site-directed mutagenesis of IL-17RB tyrosine Journal of immunology High 25681341
2015 IL-25 signals through a novel Act1-independent STAT5 pathway. STAT5 is directly activated by IL-25 and is recruited to IL-17RB in a ligand-dependent manner through unique tyrosine residues on IL-17RB. Conditional STAT5 deletion in T cells or epithelial cells leads to defective IL-25-initiated Th2 polarization. STAT5 conditional knockout mice (T cell and epithelial specific), STAT5 activation assays, receptor co-immunoprecipitation, site-directed mutagenesis of IL-17RB tyrosines, in vitro Th2 polarization assay Journal of immunology High 25821217
2015 Keratinocyte-derived IL-17E (IL-25) is increased in psoriatic plaques. Macrophages take up IL-17E via receptor-mediated clathrin-dependent endocytosis rather than synthesizing it. M2 polarized macrophages (not M1) express the IL-17E receptor and respond to IL-17E by producing inflammatory cytokines and chemokines involved in neutrophil recruitment. Immunohistochemistry of psoriatic skin biopsies, in vitro monocyte-derived macrophage polarization, endocytosis assays (clathrin inhibitor), cytokine/chemokine ELISA The Journal of investigative dermatology Medium 27329229
2017 IL-25 promotes M2 macrophage polarization, increases mitochondrial respiratory chain complex I and II/III activity and NAD+/NADH and ATP production, activates AMPK, and induces mitophagy to stimulate M2 macrophage polarization. CCL-22 secretion induced by IL-25 is suppressed by mitophagy inhibitor treatment and PINK1 knockdown. Human monocyte cell line THP-1, flow cytometry for ROS, ELISA for CCL-22, Western blot for AMPK/mitophagy proteins, confocal microscopy, mitochondrial complex activity assays, PINK1 knockdown International journal of molecular sciences Medium 35008429
2018 IL-25 enhances TH17-cell-mediated contact hypersensitivity by stimulating IL-1β production from dermal dendritic cells. Mast cell- and non-immune cell-derived IL-25 drives hapten-specific TH17 (not TH2) cell activation in the elicitation phase of contact hypersensitivity via IL-1β from dermal DCs. Il25−/− mice, CHS model (FITC), flow cytometry, ELISA for IL-1β, immunohistochemistry, bone marrow transfer experiments The Journal of allergy and clinical immunology High 29522843
2019 IL-25 (IL-17E) induces skin inflammation in vivo characterized by innate immune gene expression and neutrophil recruitment. Genetic deletion or neutralization of IL-17E ameliorates imiquimod- or tape stripping-induced skin inflammation. IL-25 promotes neutrophil recruitment via macrophage activation through a p38-dependent mechanism. Il17e−/− mice, IL-17E neutralization, imiquimod and tape stripping skin inflammation models, multi-parameter flow cytometry (tSNE-guided), in vitro macrophage-neutrophil co-culture with p38 inhibition The Journal of investigative dermatology High 30738055
2020 IL-17E (IL-25) promotes keratinocyte proliferation in 2D and 3D cultures and upregulates differentiation-associated gene transcripts (e.g., keratin 10). IL-17E increases keratinocyte cell speed and displacement, associated with changes in actin cytoskeleton organization and cell-substrate adhesion. Human keratinocytes display a complete IL-17E receptor whose expression is induced by IL-17A. IL-22 enhances IL-17E production in keratinocytes. Primary human keratinocyte culture, 2D and 3D proliferation assays, time-lapse microscopy, actin staining, flow cytometry for receptor expression, gene expression profiling The Journal of investigative dermatology Medium 31958433
2020 Keratinocyte-derived IL-25 activates ILC2s to produce IL-13, which drives epidermal hyperplasia, dermal CD4+ T cell infiltration, and expression of IL-13-dependent chemokines (Ccl17, Ccl22) at sites of allergic skin inflammation. ILCs are the major source of IL-13 in acutely sensitized skin, whereas T cells dominate in chronic sensitization. Mice lacking IL-25R, keratinocyte-specific IL-25 deletion, ILC-specific IL-25R deletion, IL-13 reporter mice (Il13-eGFP), flow cytometry, RT-qPCR, histology, OVA epicutaneous sensitization model The Journal of allergy and clinical immunology High 32179159
2020 mTOR suppresses autophagy-mediated production of IL-25 in airway epithelial cells. Allergen-induced mTOR downregulation and LC3B-dependent autophagy increase IL-25 production. MTOR-specific knockdown in bronchial epithelium augments, while LC3B deletion abolishes, allergen-induced IL-25 and subsequent airway inflammation. Blocking IL-25 attenuates exacerbated inflammation in mTOR-deficient mice. Airway epithelium-specific MTOR knockdown mice, lc3b−/− mice, allergen (OVA, HDM) challenge models, human bronchial epithelial cell assays, cytokine measurement, histology Thorax High 33077617
2021 Airway tuft cell-derived cysteinyl leukotrienes (CysLTs, specifically LTC4) and IL-25 synergistically activate ILC2s (for proliferation and cytokine production) and dendritic cells to drive type 2 lung inflammation. Tuft cell-specific deletion of Ltc4s (required for CysLT production) reduces lung inflammation and systemic immune response after aeroallergen inhalation; concomitant IL-25 blockade further enhances this reduction. LTC4-induced eosinophilia is dominantly through CysLT1R, while type 2 cytokines and innate cell activation require both CysLT1R and CysLT2R. Tuft cell-specific Ltc4s deletion, IL-25 blockade, CysLT receptor pharmacological dissection, intranasal LTC4 + subthreshold IL-25 co-administration, flow cytometry, eosinophil quantification Science immunology High 34932383
2025 IL-17E (IL-25), expressed in cortical neurons, enhances social interaction behavior by acting on IL-17RA- and IL-17RB-expressing neurons in the cortex. IL-17RB—but not IL-17RC—is expressed in the cortex and mediates social behavior effects. Brain-region-specific mapping revealed cortically restricted expression of IL-17RB. Brain-wide receptor expression mapping, genetic deletion of IL-17RB, social behavior assays, neuronal cell-type-specific expression analysis Cell Medium 40199322

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2015 Tuft-cell-derived IL-25 regulates an intestinal ILC2-epithelial response circuit. Nature 1009 26675736
2011 Human IL-25- and IL-33-responsive type 2 innate lymphoid cells are defined by expression of CRTH2 and CD161. Nature immunology 972 21909091
2001 IL-25 induces IL-4, IL-5, and IL-13 and Th2-associated pathologies in vivo. Immunity 931 11754819
2013 A role for IL-25 and IL-33-driven type-2 innate lymphoid cells in atopic dermatitis. The Journal of experimental medicine 795 24323357
2002 New IL-17 family members promote Th1 or Th2 responses in the lung: in vivo function of the novel cytokine IL-25. Journal of immunology (Baltimore, Md. : 1950) 492 12077275
2010 IL25 elicits a multipotent progenitor cell population that promotes T(H)2 cytokine responses. Nature 456 20200520
2013 IL-33 is more potent than IL-25 in provoking IL-13-producing nuocytes (type 2 innate lymphoid cells) and airway contraction. The Journal of allergy and clinical immunology 332 23810766
2007 IL-25 regulates Th17 function in autoimmune inflammation. The Journal of experimental medicine 322 17200411
2013 IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis. Proceedings of the National Academy of Sciences of the United States of America 317 24344271
2001 IL-17E, a novel proinflammatory ligand for the IL-17 receptor homolog IL-17Rh1. The Journal of biological chemistry 313 11058597
2007 Blocking IL-25 prevents airway hyperresponsiveness in allergic asthma. The Journal of allergy and clinical immunology 309 17889290
2014 Rhinovirus-induced IL-25 in asthma exacerbation drives type 2 immunity and allergic pulmonary inflammation. Science translational medicine 280 25273095
2012 IL-33, but not thymic stromal lymphopoietin or IL-25, is central to mite and peanut allergic sensitization. The Journal of allergy and clinical immunology 270 23006545
2008 Commensal-dependent expression of IL-25 regulates the IL-23-IL-17 axis in the intestine. The Journal of experimental medicine 233 18762568
2015 Recent advances in epithelium-derived cytokines (IL-33, IL-25, and thymic stromal lymphopoietin) and allergic inflammation. Current opinion in allergy and clinical immunology 196 25479313
2010 Regulation of IL-9 expression by IL-25 signaling. Nature immunology 185 20154671
2006 IL-25 enhances allergic airway inflammation by amplifying a TH2 cell-dependent pathway in mice. The Journal of allergy and clinical immunology 178 16950278
2016 Combinatorial targeting of TSLP, IL-25, and IL-33 in type 2 cytokine-driven inflammation and fibrosis. Science translational medicine 160 27147589
2017 IL-33, IL-25, and TSLP induce a distinct phenotypic and activation profile in human type 2 innate lymphoid cells. Blood advances 154 29296700
2011 Allergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses. The Journal of allergy and clinical immunology 154 21570719
2014 Neonatal rhinovirus induces mucous metaplasia and airways hyperresponsiveness through IL-25 and type 2 innate lymphoid cells. The Journal of allergy and clinical immunology 150 24910174
2001 Forced expression of murine IL-17E induces growth retardation, jaundice, a Th2-biased response, and multiorgan inflammation in mice. Journal of immunology (Baltimore, Md. : 1950) 148 11714825
2002 Transgenic overexpression of human IL-17E results in eosinophilia, B-lymphocyte hyperplasia, and altered antibody production. Blood 144 12239140
2015 IL-25 as a novel therapeutic target in nasal polyps of patients with chronic rhinosinusitis. The Journal of allergy and clinical immunology 137 25725991
2017 The Innate Cytokines IL-25, IL-33, and TSLP Cooperate in the Induction of Type 2 Innate Lymphoid Cell Expansion and Mucous Metaplasia in Rhinovirus-Infected Immature Mice. Journal of immunology (Baltimore, Md. : 1950) 132 28701507
2021 IL-25 (IL-17E) in epithelial immunology and pathophysiology. The Journal of allergy and clinical immunology 128 33485651
2011 T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma. Proceedings of the National Academy of Sciences of the United States of America 120 21205894
2015 IL-25 and CD4(+) TH2 cells enhance type 2 innate lymphoid cell-derived IL-13 production, which promotes IgE-mediated experimental food allergy. The Journal of allergy and clinical immunology 116 26560039
2013 IL-25 simultaneously elicits distinct populations of innate lymphoid cells and multipotent progenitor type 2 (MPPtype2) cells. The Journal of experimental medicine 114 23960191
2018 Bronchial Allergen Challenge of Patients with Atopic Asthma Triggers an Alarmin (IL-33, TSLP, and IL-25) Response in the Airways Epithelium and Submucosa. Journal of immunology (Baltimore, Md. : 1950) 110 30185520
2017 Prevention of food allergy development and suppression of established food allergy by neutralization of thymic stromal lymphopoietin, IL-25, and IL-33. The Journal of allergy and clinical immunology 98 28552763
2017 IL-25 in allergic inflammation. Immunological reviews 98 28658555
2021 Tuft cell-produced cysteinyl leukotrienes and IL-25 synergistically initiate lung type 2 inflammation. Science immunology 96 34932383
2013 IL-25 downregulates Th1/Th17 immune response in an IL-10-dependent manner in inflammatory bowel disease. Inflammatory bowel diseases 95 23429464
2017 IL-25 stimulates M2 macrophage polarization and thereby promotes mitochondrial respiratory capacity and lipolysis in adipose tissues against obesity. Cellular & molecular immunology 94 28194019
2011 IL-25 causes apoptosis of IL-25R-expressing breast cancer cells without toxicity to nonmalignant cells. Science translational medicine 93 21490275
2006 Mechanism of interleukin-25 (IL-17E)-induced pulmonary inflammation and airways hyper-reactivity. Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 93 17177681
2019 Intestinal dysbacteriosis-induced IL-25 promotes development of HCC via alternative activation of macrophages in tumor microenvironment. Journal of experimental & clinical cancer research : CR 92 31296243
2020 ILC2 activation by keratinocyte-derived IL-25 drives IL-13 production at sites of allergic skin inflammation. The Journal of allergy and clinical immunology 90 32179159
2011 IL-22 attenuates IL-25 production by lung epithelial cells and inhibits antigen-induced eosinophilic airway inflammation. The Journal of allergy and clinical immunology 89 21794904
2010 Overexpression of Smad2 drives house dust mite-mediated airway remodeling and airway hyperresponsiveness via activin and IL-25. American journal of respiratory and critical care medicine 83 20339149
2006 Involvement of TNF receptor-associated factor 6 in IL-25 receptor signaling. Journal of immunology (Baltimore, Md. : 1950) 83 16393988
2021 IL-25 Induced ROS-Mediated M2 Macrophage Polarization via AMPK-Associated Mitophagy. International journal of molecular sciences 82 35008429
2017 Intelectin contributes to allergen-induced IL-25, IL-33, and TSLP expression and type 2 response in asthma and atopic dermatitis. Mucosal immunology 82 28224996
2012 Epithelial cell-derived IL-25, but not Th17 cell-derived IL-17 or IL-17F, is crucial for murine asthma. Journal of immunology (Baltimore, Md. : 1950) 81 22942422
2006 IL-17E upregulates the expression of proinflammatory cytokines in lung fibroblasts. The Journal of allergy and clinical immunology 79 16522458
2009 IL-17E, a proinflammatory cytokine, has antitumor efficacy against several tumor types in vivo. Cancer immunology, immunotherapy : CII 76 20012860
2014 Clinical associations between IL-17 family cytokines and periodontitis and potential differential roles for IL-17A and IL-17E in periodontal immunity. Inflammation research : official journal of the European Histamine Research Society ... [et al.] 73 25369802
2009 Opposing roles of IL-17A and IL-25 in the regulation of TSLP production in human nasal epithelial cells. Allergy 71 19968632
2016 Keratinocyte-Derived IL-17E Contributes to Inflammation in Psoriasis. The Journal of investigative dermatology 70 27329229
2015 Mutual upregulation of endothelin-1 and IL-25 in atopic dermatitis. Allergy 70 25903653
2016 IL-25 and IL-33 induce Type 2 inflammation in basophils from subjects with allergic asthma. Respiratory research 69 26762527
2013 IL-25 and IL-25 receptor expression on eosinophils from subjects with allergic asthma. International archives of allergy and immunology 68 24247484
2009 Pulmonary IL-17E (IL-25) production and IL-17RB+ myeloid cell-derived Th2 cytokine production are dependent upon stem cell factor-induced responses during chronic allergic pulmonary disease. Journal of immunology (Baltimore, Md. : 1950) 67 19828636
2010 Protease allergens induce the expression of IL-25 via Erk and p38 MAPK pathway. Journal of Korean medical science 66 20514301
2006 IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation. Allergy 66 16792588
2018 Lung epithelial cell-derived IL-25 negatively regulates LPS-induced exosome release from macrophages. Military Medical Research 63 30056803
2022 IL-25 improves diabetic wound healing through stimulating M2 macrophage polarization and fibroblast activation. International immunopharmacology 62 35149293
2013 IL-25 enhances HSV-1 replication by inhibiting filaggrin expression, and acts synergistically with Th2 cytokines to enhance HSV-1 replication. The Journal of investigative dermatology 60 23657503
2011 Reciprocal expression of IL-25 and IL-17A is important for allergic airways hyperreactivity. Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 56 21722219
2021 Roles of IL-25 in Type 2 Inflammation and Autoimmune Pathogenesis. Frontiers in immunology 54 34122457
2017 Local IL-25 contributes to Th2-biased inflammatory profiles in nasal polyps. Allergy 54 28771767
2015 Interleukin (IL)-25: Pleiotropic roles in asthma. Respirology (Carlton, Vic.) 52 26699081
2017 House Dust Mite Increases pro-Th2 Cytokines IL-25 and IL-33 via the Activation of TLR1/6 Signaling. The Journal of investigative dermatology 51 28684329
2015 IL-17A and its homologs IL-25/IL-17E recruit the c-RAF/S6 kinase pathway and the generation of pro-oncogenic LMW-E in breast cancer cells. Scientific reports 50 26154409
2015 Association between single nucleotide polymorphisms IL17RA rs4819554 and IL17E rs79877597 and Psoriasis in a Spanish cohort. Journal of dermatological science 49 26347322
2007 Intracellular JNK, p38 MAPK and NF-kappaB regulate IL-25 induced release of cytokines and chemokines from costimulated T helper lymphocytes. Immunology letters 47 17719653
2006 TNF-alpha and IFN-gamma inversely modulate expression of the IL-17E receptor in airway smooth muscle cells. American journal of physiology. Lung cellular and molecular physiology 47 16428271
2015 IL-25 inhibits atherosclerosis development in apolipoprotein E deficient mice. PloS one 45 25629516
2019 IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation. The Journal of investigative dermatology 44 30738055
2016 IL-25 Receptor Expression on Airway Dendritic Cells after Allergen Challenge in Subjects with Asthma. American journal of respiratory and critical care medicine 44 26625138
2014 Cytokines (interleukin-9, IL-17, IL-22, IL-25 and IL-33) and asthma. Advanced biomedical research 44 24949298
2013 IL-25 prevents and cures fulminant hepatitis in mice through a myeloid-derived suppressor cell-dependent mechanism. Hepatology (Baltimore, Md.) 44 23564603
2018 IL-33, IL-25 and TSLP contribute to development of fungal-associated protease-induced innate-type airway inflammation. Scientific reports 43 30575775
2020 IL-17E (IL-25) and IL-17A Differentially Affect the Functions of Human Keratinocytes. The Journal of investigative dermatology 41 31958433
2016 IL-25 attenuates rheumatoid arthritis through suppression of Th17 immune responses in an IL-13-dependent manner. Scientific reports 41 27812008
2011 Inhibition of colitis by IL-25 associates with induction of alternatively activated macrophages. Inflammatory bowel diseases 41 21688353
2019 Combined blockade of IL-25, IL-33 and TSLP mediates amplified inhibition of airway inflammation and remodelling in a murine model of asthma. Respirology (Carlton, Vic.) 40 31610614
2014 Direct comparison of the dynamics of IL-25- and 'allergen'-induced airways inflammation, remodelling and hypersensitivity in a murine asthma model. Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 39 24575868
2008 Virulizin induces production of IL-17E to enhance antitumor activity by recruitment of eosinophils into tumors. Cancer immunology, immunotherapy : CII 39 18351336
2018 IL-25 enhances TH17 cell-mediated contact dermatitis by promoting IL-1β production by dermal dendritic cells. The Journal of allergy and clinical immunology 37 29522843
2018 Biological Properties and the Role of IL-25 in Disease Pathogenesis. Journal of immunology research 37 30345318
2022 Indolepropionic acid reduces obesity-induced metabolic dysfunction through colonic barrier restoration mediated via tuft cell-derived IL-25. The FEBS journal 36 35509122
2015 IL-25 and IL-33 Contribute to Development of Eosinophilic Airway Inflammation in Epicutaneously Antigen-Sensitized Mice. PloS one 36 26230091
2014 IL-17E (IL-25) and IL-17RB promote respiratory syncytial virus-induced pulmonary disease. Journal of leukocyte biology 36 24407884
2014 High IL-17E and low IL-17C dermal expression identifies a fibrosis-specific motif common to morphea and systemic sclerosis. PloS one 35 25136988
2014 Reciprocal regulation of lymphoid tissue development in the large intestine by IL-25 and IL-23. Mucosal immunology 35 25249168
2019 IL-25 contributes to lung fibrosis by directly acting on alveolar epithelial cells and fibroblasts. Experimental biology and medicine (Maywood, N.J.) 33 30997832
2025 Brain-wide mapping of immune receptors uncovers a neuromodulatory role of IL-17E and the receptor IL-17RB. Cell 32 40199322
2020 Interleukin (IL)-25 suppresses IL-22-induced osteoclastogenesis in rheumatoid arthritis via STAT3 and p38 MAPK/IκBα pathway. Arthritis research & therapy 32 32972460
2016 IL-22 Restrains Tapeworm-Mediated Protection against Experimental Colitis via Regulation of IL-25 Expression. PLoS pathogens 32 27055194
2017 Therapeutic efficacy of a co-blockade of IL-13 and IL-25 on airway inflammation and remodeling in a mouse model of asthma. International immunopharmacology 31 28282577
2015 Role of IL-25 in Immunity. Journal of clinical and diagnostic research : JCDR 31 26023586
2015 TRAF4-SMURF2-mediated DAZAP2 degradation is critical for IL-25 signaling and allergic airway inflammation. Journal of immunology (Baltimore, Md. : 1950) 30 25681341
2020 MTOR suppresses autophagy-mediated production of IL25 in allergic airway inflammation. Thorax 29 33077617
2015 IL-25 or IL-17E Protects against High-Fat Diet-Induced Hepatic Steatosis in Mice Dependent upon IL-13 Activation of STAT6. Journal of immunology (Baltimore, Md. : 1950) 29 26423151
2017 Efficacy of melatonin, IL-25 and siIL-17B in tumorigenesis-associated properties of breast cancer cell lines. Life sciences 28 28624391
2016 The effect of calprotectin on TSLP and IL-25 production from airway epithelial cells. Allergology international : official journal of the Japanese Society of Allergology 28 27475624
2015 A novel IL-25 signaling pathway through STAT5. Journal of immunology (Baltimore, Md. : 1950) 28 25821217
2009 IL-25: a key requirement for the regulation of type-2 immunity. BioFactors (Oxford, England) 28 19449446

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