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An endogenous caspase-11 ligand elicits interleukin-1 release from living dendritic cells
Open accessAbstract
Immune activation in context: Dendritic cells (DCs) initiate protective immunity upon binding molecules derived from microbes or released from dying cells. Zanoni et al. examined how microbial and endogenous signals interact to shape the course of the ensuing immune response (see the Perspective by Napier and Monack). They found that oxPAPC, an oxidized phospholipid released from dying cells, binds to a protein called caspase-11 in DCs, activating an inflammatory program in these cells. Whereas caspase-11 binding to oxPAPC and bacterial lipopolysaccharide causes DCs to produce the cytokine interleukin-1 (IL-1) and undergo cell death, binding to oxPAPC alone triggers DCs to secrete IL-1 and induce strong adaptive immunity. Thus, context-dependent signals can shape the ensuing immune response. Science , this issue p. 1232 ; see also p. 1173
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“at least in some cell types including DCs, CASP11 activation can drive IL-1β secretion in the absence of cell death [628].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [628]
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Self-citation
Metadata
- Authors
- Zanoni, I., Tan, Y., Di Gioia, M., Broggi, A., Ruan, J., Shi, J., Donado, C. A., Shao, F., Wu, H., Springstead, J. R., & Kagan, J. C.
- Affiliations
- Boston Children's Hospital (US)
- Harvard Medical School and Division of Gastroenterology, Boston Children’s Hospital, Boston, MA, USA.
- Harvard University (US)
- National Institute of Biological Sciences, Beijing (CN)
- Western Michigan University (US)
- Corresponding author
- Kagan, Jonathan C.
- ORCID
- Venue
- Science
- Published
- 2016-06-03
- Volume
- 352
- Issue
- 6290
- Pages
- 1232-1236
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC5111085
- OpenAlex
- W2340046691
- Cited by
- 583
- References
- 30
- Citations by year
- 2026: 34 · 2025: 69 · 2024: 58 · 2023: 76 · 2022: 69 · 2021: 62 · 2020: 61 · 2019: 51 · 2018: 49 · 2017: 38 · 2016: 14
- FWCI
- 26.34
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- BOA (University of Milano-Bicocca) (submittedVersion)
- Funders
- Mead Johnson & Company
- Burroughs Wellcome Fund
- Harvard Digestive Diseases Center (P30 DK34854)
- Cariplo Foundation
- Jane Coffin Childs Fund
- NIH (AI093589, AI072955, P30 DK34854, 1R01AI121066-01A1, 1R15HL121770-01A1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- caspase-11, dendritic cells, OxPAPC, lipopolysaccharide, pyroptosis, inflammasome, dendritic cell activation, pattern recognition receptors, innate immunity, adaptive immune response
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Carrier Proteins, Dendritic Cells, Immunity, Innate, Lipopolysaccharides, Phospholipids, Cell Death, Mice, Knockout, Caspases, Receptors, Pattern Recognition, Toll-Like Receptor 4, Mice, Caspases, Initiator, Interleukin-1beta, Adaptive Immunity, Inflammasomes
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