期刊
IMMUNITY
卷 53, 期 3, 页码 533-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2020.07.004
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资金
- Australian National Health and Medical Research Council (NHMRC) [1186575, 1145728, 1143105, 1159658, 1016701, 1020363, 1156095]
- Leukemia and Lymphoma Society of America [LLS SCOR 700113]
- Cancer Council of Victoria [1147328, 1052309]
- Australian Phenomics Network
- Cass Foundation
- Wellcome Trust [108045/Z/15/Z]
- German Research Council [GRK2168]
- Victorian State Government Operational Infrastructure Support Program
- Australian Government Independent Research Institute Infrastructure Support Scheme [361646, 9000220]
- National Health and Medical Research Council of Australia [1186575, 1159658] Funding Source: NHMRC
Programmed cell death contributes to host defense against pathogens. To investigate the relative importance of pyroptosis, necroptosis, and apoptosis during Salmonella infection, we infected mice and macrophages deficient for diverse combinations of caspases-1, -11, -12, and -8 and receptor interacting serine/threonine kinase 3 (RIPK3). Loss of pyroptosis, caspase-8-driven apoptosis, or necroptosis had minor impact on Salmonella control. However, combined deficiency of these cell death pathways caused loss of bacterial control in mice and their macrophages, demonstrating that host defense can employ varying components of several cell death pathways to limit intracellular infections. This flexible use of distinct cell death pathways involved extensive cross-talk between initiators and effectors of pyroptosis and apoptosis, where initiator caspases-1 and -8 also functioned as executioners when all known effectors of cell death were absent. These findings uncover a highly coordinated and flexible cell death system with in-built fail-safe processes that protect the host from intracellular infections.
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