ArticleThe Journal of experimental medicine1998
Production of mice deficient in genes for interleukin (IL)-1alpha, IL-1beta, IL-1alpha/beta, and IL-1 receptor antagonist shows that IL-1beta is crucial in turpentine-induced fever development and glucocorticoid secretion.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers.
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257 citing papers in PubMed, 613 citations in OpenAlex.
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- Aurora A exacerbates antibiotic-resistant Staphylococcus aureus infection through ASC phosphorylation.EMBO reports · 2026Article
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- An IL-1, IL-17, and IL-22 cytokine circuit controls vulvovaginal candidiasis independently of estrogen.PLoS pathogens · 2026Article
- IL-1 delineates squalene-based adjuvant efficacy and reactogenicity in a cell-type-specific manner.NPJ vaccines · 2026Article
- Nerve Injury-Induced Immune Responses in the Taste Bud Target Field.International journal of molecular sciences · 2026Article
- Common clonal hematopoiesis driver mutations have disparate effects on macrophage cytokines, clonal expansion, and atherogenesis.JCI insight · 2026Article
- Evaluation of the Effect of IL-1 Antagonists on Pituitary Function.International journal of endocrinology · 2026Article
- Cancer cell-derived IL-1β reverses chemo-immunotherapy resistance in non-small cell lung cancer.Nature communications · 2025Article
- B cells inhibit IL-1 family cytokine production and Mycobacterium tuberculosis growth in human CD14+ cells.ImmunoHorizons · 2025Article
- The N-terminal domain of precursor IL-1α enhances IL-6 expression via an intracrine mechanism in oral squamous cell carcinoma.Molecular biology reports · 2025Article
- Modelling the ageing dependence of cancer evolutionary trajectories.Nature reviews. Cancer · 2025Review
- Aqueous extract ofBiochemistry and biophysics reports · 2025Article
- Heparan sulfate fine-tuned interleukin-1 (IL-1) signaling inhibits insulin secretion of grafted pancreatic islets.Science advances · 2025Article
- IL-33-primed NLRP3 inflammasome in basophils drives IL-1β production and initiates atopic dermatitis inflammation.Cell death discovery · 2025Article
- Dietary fermentable polyols fuel gut inflammation through M1 macrophage polarization and gut microbiota.iScience · 2025Article
- NLRP3 inflammasome-driven hemophagocytic lymphohistiocytosis occurs independent of IL-1β and IL-18 and is targetable by BET inhibitors.Science advances · 2025Article
- IL-1 protects from fatal systemic candidiasis in mice by inhibiting oxidative phosphorylation and hypoxia.Nature communications · 2025Article
- A Review of Key Regulators of Steady-State and Ineffective Erythropoiesis.Journal of clinical medicine · 2024Review
197 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-1 is a major mediator of inflammation and exerts pleiotropic effects on the neuro-immuno-endocrine system. To elucidate pathophysiological roles of IL-1, we have first produced IL-1alpha/beta doubly deficient (KO) mice together with mice deficient in either the IL-1alpha, IL-1beta, or IL-1 receptor antagonist (IL-1ra) genes. These mice were born healthy, and their growth was normal except for IL-1ra KO mice, which showed growth retardation after weaning. Fever development upon injection with turpentine was suppressed in IL-1beta as well as IL-1alpha/beta KO mice, but not in IL-1alpha KO mice, whereas IL-1ra KO mice showed an elevated response. At this time, expression of IL-1beta mRNA in the diencephalon decreased 1.5-fold in IL-1alpha KO mice, whereas expression of IL-1alpha mRNA decreased >30-fold in IL-1beta KO mice, suggesting mutual induction between IL-1alpha and IL-1beta. This mutual induction was also suggested in peritoneal macrophages stimulated with lipopolysaccharide in vitro. In IL-1beta KO mice treated with turpentine, the induction of cyclooxygenase-2 (EC 1.14.99.1) in the diencephalon was suppressed, whereas it was enhanced in IL-1ra KO mice. We also found that glucocorticoid induction 8 h after turpentine treatment was suppressed in IL-1beta but not IL-1alpha KO mice. These observations suggest that IL-1beta but not IL-1alpha is crucial in febrile and neuro-immuno-endocrine responses, and that this is because IL-1alpha expression in the brain is dependent on IL-1beta. The importance of IL-1ra both in normal physiology and under stress is also suggested.
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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.