Evidence map›Paper›PMID 30940725›Full record

ArticleThe Journal of biological chemistry2019

The three cytokines IL-1β, IL-18, and IL-1α share related but distinct secretory routes.

Victor S Tapia, Michael J D Daniels, Pablo Palazón-Riquelme, Matthew Dewhurst, Nadia M Luheshi, Jack Rivers-Auty, Jack Green, Elena Redondo-Castro, Philipp Kaldis, Gloria Lopez-Castejon and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 87 citations in OpenAlex.

  1. An ancient evolutionary origin for IL-1 cytokines.Nature ecology & evolution · 2026
    Article
  2. Article
  3. Fibroblasts resistScience advances · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. How can we balance risk and benefit of interleukin-18 armored T cell therapies?Experimental biology and medicine (Maywood, N.J.) · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. CXCL14 Chemokine Exacerbates Acute Viral Hepatitis in Coronavirus MHV-Infected Mice and Is Associated With Human Acute Viral Hepatitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 3 countries.

Victor S TapiaLydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PT, United Kingdom; Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, AV Hill Building, Oxford Road, Manchester M13 9PT, United Kingdom.
Michael J D DanielsDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, AV Hill Building, Oxford Road, Manchester M13 9PT, United Kingdom; UK Dementia Research Institute, University of Edinburgh, College of Medicine and Veterinary Medicine, 49 Little France Crescent, Edinburgh EH16 4SB, Scotland, United Kingdom.
Pablo Palazón-RiquelmeDivision of Infection, Immunity, and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Collaborative Centre of Inflammation Research, Manchester Academic Health Science Centre, Core Technology Facility, University of Manchester, Manchester M13 9PT, United Kingdom; International Centre for Infectiology Research, INSERM U1111, CNRS UMR5308, École Normale Supérieure de Lyon, Claude Bernard Lyon 1 University, 69100 Lyon, France.
Matthew DewhurstDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, AV Hill Building, Oxford Road, Manchester M13 9PT, United Kingdom; Institute of Molecular and Cell Biology (IMCB), A*STAR (Agency for Science, Technology and Research), Department of Biochemistry, National University of Singapore (NUS), Singapore 119007, Singapore.
Nadia M LuheshiDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, AV Hill Building, Oxford Road, Manchester M13 9PT, United Kingdom; MedImmune Ltd., Aaron Klug Building, Granta Park, Cambridge CB21 6GH, United Kingdom.
Jack Rivers-AutyLydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PT, United Kingdom; Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, AV Hill Building, Oxford Road, Manchester M13 9PT, United Kingdom.
Jack GreenLydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PT, United Kingdom; Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, AV Hill Building, Oxford Road, Manchester M13 9PT, United Kingdom.
Elena Redondo-CastroDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, AV Hill Building, Oxford Road, Manchester M13 9PT, United Kingdom.
Philipp KaldisInstitute of Molecular and Cell Biology (IMCB), A*STAR (Agency for Science, Technology and Research), Department of Biochemistry, National University of Singapore (NUS), Singapore 119007, Singapore.
Gloria Lopez-CastejonLydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PT, United Kingdom; Division of Infection, Immunity, and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Collaborative Centre of Inflammation Research, Manchester Academic Health Science Centre, Core Technology Facility, University of Manchester, Manchester M13 9PT, United Kingdom. Electronic address: Gloria.lopez-castejon@manchester.ac.uk.
David BroughLydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PT, United Kingdom; Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, AV Hill Building, Oxford Road, Manchester M13 9PT, United Kingdom. Electronic address: david.brough@manchester.ac.uk.
Manchester Academic Health Science Centre · GBAgency for Science, Technology and Research · SGUniversité Claude Bernard Lyon 1 · FR

Funding

Biotechnology and Biological Sciences Research Council BB/P01061X/1Medical Research Council MR/K501311/1Medical Research Council MR/N029992/1Wellcome TrustWellcome Trust 104192/Z/14/Z
6 · The paper itself

Abstract

Interleukin (IL)-1 family cytokines potently regulate inflammation, with the majority of the IL-1 family proteins being secreted from immune cells via unconventional pathways. In many cases, secretion of IL-1 cytokines appears to be closely coupled to cell death, yet the secretory mechanisms involved remain poorly understood. Here, we studied the secretion of the three best-characterized members of the IL-1 superfamily, IL-1α, IL-1β, and IL-18, in a range of conditions and cell types, including murine bone marrow-derived and peritoneal macrophages, human monocyte-derived macrophages, HeLa cells, and mouse embryonic fibroblasts. We discovered that IL-1β and IL-18 share a common secretory pathway that depends upon membrane permeability and can operate in the absence of complete cell lysis and cell death. We also found that the pathway regulating the trafficking of IL-1α is distinct from the pathway regulating IL-1β and IL-18. Although the release of IL-1α could also be dissociated from cell death, it was independent of the effects of the membrane-stabilizing agent punicalagin, which inhibited both IL-1β and IL-18 release. These results reveal that in addition to their role as danger signals released from dead cells, IL-1 family cytokines can be secreted in the absence of cell death. We propose that models used in the study of IL-1 release should be considered context-dependently.

Indexed as

AnimalsBone Marrow CellsFibroblastsHeLa CellsHumansHydrolyzable TanninsInterleukin-18Interleukin-1alphaInterleukin-1betaMacrophages, PeritonealMiceProtein TransportHydrolyzable TanninsIL1A protein, humanIL1B protein, humanIL1B protein, mouseInterleukin-18Interleukin-1alphaInterleukin-1betapunicalagincalpaincaspase 1 (CASP1)cytokineimmune cellimmunologyinflammasomeinflammationinterleukin 1 (IL-1)neutrophilNLRP3

Identifiers

PMID30940725
PMCPMC6544845
OpenAlexW2934583654

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.