| First Author | Yow SJ | Year | 2024 |
| Journal | Cell Death Dis | Volume | 15 |
| Issue | 7 | Pages | 479 |
| PubMed ID | 38965211 | Mgi Jnum | J:360392 |
| Mgi Id | MGI:7664764 | Doi | 10.1038/s41419-024-06871-8 |
| Citation | Yow SJ, et al. (2024) Differential signalling requirements for RIPK1-dependent pyroptosis in neutrophils and macrophages. Cell Death Dis 15(7):479 |
| abstractText | 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-gamma 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. |
