ArticleThe Journal of experimental medicine2017
Leukotrienes provide an NFAT-dependent signal that synergizes with IL-33 to activate ILC2s.
Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
107 citing papers in PubMed, 169 citations in OpenAlex.
- Platelet-macrophage cooperation drives IL-33-dependent type 2 lung immunopathology in a sex-biased manner.The Journal of allergy and clinical immunology · 2026Article
- Review
- Single-cell analysis of recruited ILC2 cell fate during transition from circulation to establishment of tissue residency.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Disturbed LTB4 Metabolism in ILC2s Aggravates Ulcerative Colitis via Intercellular ATP Accumulation.Inflammation · 2026Article
- Effects of MK-886, an inhibitor of the 5-lipoxygenase-activating protein, on peripheral blood mononuclear cells from patients with Chagas' heart disease.Revista da Sociedade Brasileira de Medicina Tropical · 2026Article
- Using gnotobiotic mice to decipher effects of gut microbiome repair in undernourished children on tuft and goblet cell function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unraveling cysteinyl leukotrienes and their receptors in inflammation through the brain-gut-lung axis.Virulence · 2025Review
- The immunoproteasome regulates ILC2 responses by modulating mitochondrial capacity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Using gnotobiotic mice to decipher effects of gut microbiome repair in undernourished children on tuft and goblet cell function.bioRxiv : the preprint server for biology · 2025Article
- New Perspectives on Classical Alarmin Responses to Intestinal Helminth Infection.Parasite immunology · 2025Review
- Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens.Science (New York, N.Y.) · 2025Article
- The immunology of asthma and chronic rhinosinusitis.Nature reviews. Immunology · 2025Review
- Decoding innate lymphoid cells and innate-like lymphocytes in asthma: pathways to mechanisms and therapies.Journal of biomedical science · 2025Review
- Genetics of helminth infections: Immune system response, insights into host-parasite interaction, and drug resistance.Journal of advanced veterinary and animal research · 2025Article
- Tissue-Specific Metabolic Reprogramming in Innate Lymphoid Cells and Its Impact on Disease.Immune network · 2025Review
- The epidermal lipid-microbiome loop and immunity: Important players in atopic dermatitis.Journal of advanced research · 2025Review
- Cysteinyl Leukotrienes in Allergic Inflammation.Annual review of pathology · 2025Review
- Tuft cell cysteinyl leukotrienes are necessary for rhinovirus-induced mucus metaplasia, type 2 inflammation and airway hyperresponsiveness in immature mice.Frontiers in immunology · 2025Article
- Beyond CCR7: dendritic cell migration in type 2 inflammation.Frontiers in immunology · 2025Review
- A mouse protozoan boosts antigen-specific mucosal IgA responses in a specific lipid metabolism- and signaling-dependent manner.Nature communications · 2024Article
47 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
6 authors at 2 institutions in 1 country.
Funding
Abstract
Group 2 innate lymphoid cells (ILC2s) and type 2 helper T cells (Th2 cells) are the primary source of interleukin 5 (IL-5) and IL-13 during type 2 (allergic) inflammation in the lung. In Th2 cells, T cell receptor (TCR) signaling activates the transcription factors nuclear factor of activated T cells (NFAT), nuclear factor κB (NF-κB), and activator protein 1 (AP-1) to induce type 2 cytokines. ILC2s lack a TCR and respond instead to locally produced cytokines such as IL-33. Although IL-33 induces AP-1 and NF-κB, NFAT signaling has not been described in ILC2s. In this study, we report a nonredundant NFAT-dependent role for lipid-derived leukotrienes (LTs) in the activation of lung ILC2s. Using cytokine reporter and LT-deficient mice, we find that complete disruption of LT signaling markedly diminishes ILC2 activation and downstream responses during type 2 inflammation. Type 2 responses are equivalently attenuated in IL-33- and LT-deficient mice, and optimal ILC2 activation reflects potent synergy between these pathways. These findings expand our understanding of ILC2 regulation and may have important implications for the treatment of airways disease.
Indexed as
Identifiers
What OpenQuestion holds
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.