ArticleImmunity2017
Epidermal Growth Factor Receptor Expression Licenses Type-2 Helper T Cells to Function in a T Cell Receptor-Independent Fashion.
Article in Immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
66 citing papers in PubMed, 105 citations in OpenAlex.
- Multiomic analysis identifies T cell subsets and mechanisms of epithelial interaction in idiopathic pulmonary fibrosis.JCI insight · 2026Article
- Pathogenic type-2 immunity beyond allergy: the role of Th2 cell heterogeneity in helminth infections.Infection and immunity · 2026Review
- The Epidermal Growth Factor Receptor (EGFR) as a means of neuro-immune cross-conversation.Journal of neuroinflammation · 2026Review
- IL-33 promotes transcriptional and metabolic adaptations of tissue-resident Th2 cells.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Distinguishing Features of ILC2s During Type 2 Immune Responses.European journal of immunology · 2026Review
- Regulatory T Cells in Diabetic Wound Healing: A Comprehensive Review.Journal of inflammation research · 2026Review
- High-Throughput De Novo Protein Design Yields Novel Immunomodulatory Agonists.bioRxiv : the preprint server for biology · 2025Article
- Macrophage-derived amphiregulin induces myofibroblast transition in adipogenic lineage precursors near Staphylococcus aureus abscess in bone marrow.Nature communications · 2025Article
- New Perspectives on Classical Alarmin Responses to Intestinal Helminth Infection.Parasite immunology · 2025Review
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- Breaking barriers: Smart vaccine platforms for cancer immunomodulation.Cancer communications (London, England) · 2025Review
- Tissue-Resident Th2 Cells in Type 2 Immunity and Allergic Diseases.Immunological reviews · 2025Review
- Terminal differentiation and persistence of effector regulatory T cells essential for preventing intestinal inflammation.Nature immunology · 2025Article
- EGF receptor in organ development, tissue homeostasis and regeneration.Journal of biomedical science · 2025Review
- The amphiregulin- epidermal growth factor receptor axis as a therapeutic target in sepsis.Frontiers in immunology · 2025Observational
- Mast Cells Promote Inflammatory Th17 Cells and Impair Treg Cells Through an IL-1β and PGEJournal of inflammation research · 2025Article
- Therapeutic monoclonal antibodies in allergy: Targeting IgE, cytokine, and alarmin pathways.Immunological reviews · 2024Review
- Systemic Immune Modulation by Gastrointestinal Nematodes.Annual review of immunology · 2024Review
- Cooperation of ILC2s and TNature reviews. Immunology · 2024Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 5 countries.
Funding
Abstract
Gastro-intestinal helminth infections trigger the release of interleukin-33 (IL-33), which induces type-2 helper T cells (Th2 cells) at the site of infection to produce IL-13, thereby contributing to host resistance in a T cell receptor (TCR)-independent manner. Here, we show that, as a prerequisite for IL-33-induced IL-13 secretion, Th2 cells required the expression of the epidermal growth factor receptor (EGFR) and of its ligand, amphiregulin, for the formation of a signaling complex between T1/ST2 (the IL-33R) and EGFR. This shared signaling complex allowed IL-33 to induce the EGFR-mediated activation of the MAP-kinase signaling pathway and consequently the expression of IL-13. Lack of EGFR expression on T cells abrogated IL-13 expression in infected tissues and impaired host resistance. EGFR expression on Th2 cells was TCR-signaling dependent, and therefore, our data reveal a mechanism by which antigen presentation controls the innate effector function of Th2 cells at the site of inflammation.
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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.