Cited by 564Inflammasome and immune disordersAdenosine and Purinergic SignalingImmune Response and Inflammation

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Nonclassical IL-1β Secretion Stimulated by P2X7 Receptors Is Dependent on Inflammasome Activation and Correlated with Exosome Release in Murine Macrophages

Qu, Yan, Franchi, Luigi, Nunez, Gabriel, Dubyak, George R·2007·The Journal of Immunology

DOI 10.4049/jimmunol.179.3.1913

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Abstract

Several mechanistically distinct models of nonclassical secretion, including exocytosis of secretory lysosomes, shedding of plasma membrane microvesicles, and direct efflux through plasma membrane transporters, have been proposed to explain the rapid export of caspase-1-processed IL-1β from monocytes/macrophages in response to activation of P2X7 receptors (P2X7R) by extracellular ATP. We compared the contribution of these mechanisms to P2X7R-stimulated IL-1β secretion in primary bone marrow-derived macrophages isolated from wild-type, P2X7R knockout, or apoptosis-associated speck-like protein containing a C-terminal CARD knockout mice. Our experiments revealed the following: 1) a novel correlation between IL-1β secretion and the release of the MHC-II membrane protein, which is a marker of plasma membranes, recycling endosomes, multivesicular bodies, and released exosomes; 2) a common and absolute requirement for inflammasome assembly and active caspase-1 in triggering the cotemporal export of IL-1β and MHC-II; and 3) mechanistic dissociation of IL-1β export from either secretory lysosome exocytosis or plasma membrane microvesicle shedding on the basis of different requirements for extracellular Ca2+ and differential sensitivity to pharmacological agents that block activation of caspase-1 inflammasomes. Thus, neither secretory lysosome exocytosis nor microvesicle shedding models constitute the major pathways for nonclassical IL-1β secretion from ATP-stimulated murine macrophages. Our findings suggest an alternative model of IL-1β release that may involve the P2X7R-induced formation of multivesicular bodies that contain exosomes with entrapped IL-1β, caspase-1, and other inflammasome components.

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Authors: Qu, Y., Franchi, L., Nunez, G., & Dubyak, G. R.
Affiliations: Case Western Reserve University (US)
University of Michigan (US)
Department of Pathology, University of Michigan , Ann Arbor, MI 48109
ORCID: Qu, Yan
Dubyak, George R
Venue: The Journal of Immunology
Publisher: Oxford University Press (OUP)
Published: 2007-08-01
Volume: 179
Issue: 3
Pages: 1913-1925
ISSN: 0022-1767 (ISSN-L)
1550-6606
DOI: 10.4049/jimmunol.179.3.1913
OpenAlex: W2100358971
Cited by: 563
References: 75
Citations by year: 2026: 16 · 2025: 21 · 2024: 21 · 2023: 26 · 2022: 24 · 2021: 27 · 2020: 36 · 2019: 28 · 2018: 36 · 2017: 30 · 2016: 30 · 2015: 43 · 2014: 37 · 2013: 36 · 2012: 38
FWCI: 9.93
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: The Journal of Immunology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of General Medical Sciences (GM-36387, R01GM036387)
National Institute of Allergy and Infectious Diseases (AI 064748, AI063331, R01AI064748)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: P2X7 receptor, inflammasome, caspase-1, exosomes, macrophages, extracellular ATP, multivesicular bodies, extracellular calcium
MeSH terms: Adenosine Triphosphate, Animals, Cathepsin B, Cells, Cultured, Enzyme Activation, Exocytosis, Inflammation, Lysosomes, Macrophages, Mice, Inbred BALB C, Mice, Inbred C57BL, Endosomes, Signal Transduction, Receptors, Purinergic P2, Mice, Knockout, Models, Immunological, Caspase 1, Multiprotein Complexes, Mice, Interleukin-1beta, Receptors, Purinergic P2X7

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Nonclassical IL-1β Secretion Stimulated by P2X7 Receptors Is Dependent on Inflammasome Activation and Correlated with Exosome Release in Murine Macrophages

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