ArticleMucosal immunology2013
Potential autocrine regulation of interleukin-33/ST2 signaling of dendritic cells in allergic inflammation.
Article in Mucosal immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 78 citations in OpenAlex.
- Elevated interleukin-33, CD1c+ dendritic cells, and interleukin-17A in peritoneal fluid of patients with endometriosis: a case-control study.Molecular biology reports · 2026Article
- RTA-408 Regulates p-NF-κB/TSLP/STAT5 Signaling to Ameliorate Nociceptive Hypersensitivity in Chronic Constriction Injury Rats.Molecular neurobiology · 2024Article
- Effect of three clinical therapies on cytokines modulation in the hip articular cartilage and bone improvement in rat early osteonecrosis of the femoral head.Biomedical journal · 2023Article
- Impact of Exposomes on Ocular Surface Diseases.International journal of molecular sciences · 2023Review
- Dendritic cells drive profibrotic inflammation and aberrant T cell polarization in systemic sclerosis.Rheumatology (Oxford, England) · 2023Article
- A CpG-Oligodeoxynucleotide Suppresses Th2/Th17 Inflammation by Inhibiting IL-33/ST2 Signaling in Mice from a Model of Adoptive Dendritic Cell Transfer of Smoke-Induced Asthma.International journal of molecular sciences · 2023Article
- The Role of the Interleukin-1 Family in Complications of Prematurity.International journal of molecular sciences · 2023Review
- Intestinal factors promoting the development of RORγtFrontiers in immunology · 2023Review
- Orchestrated regulation of immune inflammation with cell therapy in pediatric acute liver injury.Frontiers in immunology · 2023Review
- Linalyl Acetate Ameliorates Mechanical Hyperalgesia Through Suppressing Inflammation by TSLP/IL-33 Signaling.Neurochemical research · 2022Article
- Review
- Review
- Involvement of IL-33 in the Pathophysiology of Systemic Lupus Erythematosus: Review.International journal of molecular sciences · 2022Review
- Review
- Adipose-mesenchymal stromal cells suppress experimental Sjögren syndrome by IL-33-driven expansion of ST2iScience · 2021Article
- IL-33 in Rheumatic Diseases.Frontiers in medicine · 2021Review
- Egg yolk augments type 2 immunity by activating innate cells.European journal of nutrition · 2020Article
- Role of myeloid cells in the regulation of group 2 innate lymphoid cell-mediated allergic inflammation.Immunology · 2020Review
- Article
- Ovalbumin-Derived Peptides Activate Retinoic Acid Signalling Pathways and Induce Regulatory Responses Through Toll-Like Receptor Interactions.Nutrients · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
This study identified a novel phenomenon that dendritic cells (DCs) produced interleukin (IL)-33 via Toll-like receptor (TLR)-mediated innate pathway. Mouse bone marrow-derived DCs were treated with or without microbial pathogens or recombinant murine IL-33. IL-33 mRNA and protein were found to be expressed by DCs and largely induced by several microbial pathogens, highly by lipopolysaccharide (LPS) and flagellin. Using two mouse models of topical challenge by LPS and flagellin and experimental allergic conjunctivitis, IL-33-producing DCs were observed in ocular mucosal surface and the draining cervical lymph nodes in vivo. The increased expression levels of myeloid differentiation primary-response protein 88 (MyD88), nuclear factor (NF)-κB1, NF-κB2, and RelA accompanied by NF-κB p65 nuclear translocation were observed in DCs exposed to flagellin. IL-33 induction by flagellin was significantly blocked by TLR5 antibody or NF-κB inhibitor quinazoline and diminished in DCs from MyD88 knockout mice. IL-33 stimulated the expression of DC maturation markers, CD40 and CD80, and proallergic cytokines and chemokines, OX40L, IL-4, IL-5, IL-13, CCL17 (C-C motif chemokine ligand 17), TNF-α (tumor necrosis factor-α), and IL-1β. This stimulatory effect of IL-33 in DCs was significantly blocked by ST2 antibody or soluble ST2. Our findings demonstrate that DCs produce IL-33 via TLR/NF-κB signaling pathways, suggesting a molecular mechanism by which local allergic inflammatory response may be amplified by DC-produced IL-33 through potential autocrine regulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.