Differential signalling requirements for RIPK1-dependent pyroptosis in neutrophils and macrophages

TLR4 and TNFR1 signalling promotes potent proinflammatory signal transduction events, thus, are often hijacked by pathogenic microorganisms. We recently reported that myeloid cells retaliate Yersinia blockade of TAK1/IKK signalling by triggering RIPK1-dependent caspase-8 activation that promotes dow...

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Bibliographic Details
Published in:	Cell death & disease Vol. 15; no. 7; pp. 479 - 8
Main Authors:	Yow, See Jie, Rosli, Safwah Nasuha, Hutchinson, Paul E., Chen, Kaiwen W.
Format:	Journal Article
Language:	English
Published:	London Nature Publishing Group UK 04-07-2024 Springer Nature B.V Nature Publishing Group
Subjects:	13/2 631/250/1933 631/250/254 96 Adaptor Proteins, Vesicular Transport - metabolism Animals Antibodies Autocrine signalling Biochemistry Biomedical and Life Sciences Caspase-8 Cell activation Cell Biology Cell Culture Cell death Cytokines Immunology Inflammation Interferon-gamma - metabolism Leukocytes (neutrophilic) Life Sciences Macrophages Macrophages - metabolism Mice Mice, Inbred C57BL Mice, Knockout Myeloid cells Neutrophils Neutrophils - metabolism Pyroptosis Receptor-Interacting Protein Serine-Threonine Kinases - genetics Receptor-Interacting Protein Serine-Threonine Kinases - metabolism Receptors, Tumor Necrosis Factor, Type I - metabolism Signal Transduction TAK1 protein TLR4 protein Toll-Like Receptor 4 - metabolism Toll-like receptors Tumor necrosis factor receptors Yersinia γ-Interferon
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Summary:	TLR4 and TNFR1 signalling promotes potent proinflammatory signal transduction events, thus, are often hijacked by pathogenic microorganisms. We recently reported that myeloid cells retaliate Yersinia blockade of TAK1/IKK signalling by triggering RIPK1-dependent caspase-8 activation that promotes downstream GSDMD and GSDME-mediated pyroptosis in macrophages and neutrophils respectively. However, the upstream signalling events for RIPK1 activation in these cells are not well defined. Here, we demonstrate that unlike in macrophages, RIPK1-driven pyroptosis and cytokine priming in neutrophils are driven through TNFR1 signalling, while TLR4-TRIF signalling is dispensable. Furthermore, we demonstrate that activation of RIPK1-dependent pyroptosis in neutrophils during Yersinia infection requires IFN-γ priming, which serves to induce surface TNFR1 expression and amplify soluble TNF secretion. In contrast, macrophages utilise both TNFR1 and TLR4-TRIF signalling to trigger cell death, but only require TRIF but not autocrine TNFR1 for cytokine production. Together, these data highlight the emerging theme of cell type-specific regulation in cell death and immune signalling in myeloid cells.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	2041-4889 2041-4889
DOI:	10.1038/s41419-024-06871-8