The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Innate immune priming in the absence of TAK1 drives RIPK1 kinase activity–independent pyroptosis, apoptosis, necroptosis, and inflammatory disease
Open accessAbstract
RIPK1 kinase activity has been shown to be essential to driving pyroptosis, apoptosis, and necroptosis. However, here we show a kinase activity–independent role for RIPK1 in these processes using a model of TLR priming in a TAK1-deficient setting to mimic pathogen-induced priming and inhibition. TLR priming of TAK1-deficient macrophages triggered inflammasome activation, including the activation of caspase-8 and gasdermin D, and the recruitment of NLRP3 and ASC into a novel RIPK1 kinase activity–independent cell death complex to drive pyroptosis and apoptosis. Furthermore, we found fully functional RIPK1 kinase activity–independent necroptosis driven by the RIPK3–MLKL pathway in TAK1-deficient macrophages. In vivo, TAK1 inactivation resulted in RIPK3–caspase-8 signaling axis–driven myeloid proliferation and a severe sepsis-like syndrome. Overall, our study highlights a previously unknown mechanism for RIPK1 kinase activity–independent inflammasome activation and pyroptosis, apoptosis, and necroptosis (PANoptosis) that could be targeted for treatment of TAK1-associated myeloid proliferation and sepsis.
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Citations
Cites
Structure, function and diversity of the healthy human microbiome
The Human Microbiome Project Consortium (2012) · Nature · doi:10.1038/nature11234 · Cited by 11,726
Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death
Shi, J., Zhao, Y., Wang, K., Shi, X., Wang, Y., Huang, H., Zhuang, Y., Cai, T., Wang, F., & Shao, F. (2015) · Nature · doi:10.1038/nature15514 · Cited by 6,659
Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling
Kayagaki, N., Stowe, I. B., Lee, B. L., O’Rourke, K., Anderson, K., Warming, S., Cuellar, T., Haley, B., Roose-Girma, M., Phung, Q. T., et al. (2015) · Nature · doi:10.1038/nature15541 · Cited by 3,686
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Catalytic activity of the caspase-8–FLIPL complex inhibits RIPK3-dependent necrosis
Oberst, A., Dillon, C. P., Weinlich, R., McCormick, L. L., Fitzgerald, P., Pop, C., Hakem, R., Salvesen, G. S., & Green, D. R. (2011) · Nature · doi:10.1038/nature09852 · Cited by 1,278
Bacterial RNA and small antiviral compounds activate caspase-1 through cryopyrin/Nalp3
Kanneganti, T.-D., Özören, N., Body-Malapel, M., Amer, A., Park, J.-H., Franchi, L., Whitfield, J., Barchet, W., Colonna, M., Vandenabeele, P., et al. (2006) · Nature · doi:10.1038/nature04517 · Cited by 1,148
Self-citationThe Death Domain Kinase RIP Mediates the TNF-Induced NF-κB Signal
Kelliher, M. A., Grimm, S., Ishida, Y., Kuo, F., Stanger, B. Z., & Leder, P. (1998) · Immunity · doi:10.1016/s1074-7613(00)80535-x · Cited by 1,102
RIP3 mediates the embryonic lethality of caspase-8-deficient mice
Kaiser, W. J., Upton, J. W., Long, A. B., Livingston-Rosanoff, D., Daley-Bauer, L. P., Hakem, R., Caspary, T., & Mocarski, E. S. (2011) · Nature · doi:10.1038/nature09857 · Cited by 1,057
Pathogen blockade of TAK1 triggers caspase-8–dependent cleavage of gasdermin D and cell death
Orning, P., Weng, D., Starheim, K., Ratner, D., Best, Z., Lee, B., Brooks, A., Xia, S., Wu, H., Kelliher, M. A., et al. (2018) · Science · doi:10.1126/science.aau2818 · Cited by 1,029
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Cited by
Karki, R., Sharma, B. R., Tuladhar, S., Williams, E. P., Zalduondo, L., Samir, P., Zheng, M., Sundaram, B., Banoth, B., Malireddi, R. K. S., et al. (2021) · Cell · doi:10.1016/j.cell.2020.11.025 · Cited by 1,734
Self-citationAn update on the regulatory mechanisms of NLRP3 inflammasome activation
Paik, S., Kim, J. K., Silwal, P., Sasakawa, C., & Jo, E.-K. (2021) · Cellular & Molecular Immunology · doi:10.1038/s41423-021-00670-3 · Cited by 892
Zheng, M., & Kanneganti, T. (2020) · Immunological Reviews · doi:10.1111/imr.12909 · Cited by 586
Self-citationChristgen, S., Zheng, M., Kesavardhana, S., Karki, R., Malireddi, R. K. S., Banoth, B., Place, D. E., Briard, B., Sharma, B. R., Tuladhar, S., et al. (2020) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2020.00237 · Cited by 588
Self-citationSamir, P., Malireddi, R. K. S., & Kanneganti, T.-D. (2020) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2020.00238 · Cited by 557
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Metadata
- Authors
- Malireddi, R. K. S., Gurung, P., Kesavardhana, S., Samir, P., Burton, A., Mummareddy, H., Vogel, P., Pelletier, S., Burgula, S., & Kanneganti, T.-D.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2019-12-23
- Volume
- 217
- Issue
- 3
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2998122367
- Cited by
- 384
- References
- 45
- FWCI
- 8.16
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Malireddi, R. K. S., Gurung, P., Kesavardhana, S., Samir, P., Burton, A., Mummareddy, H., Vogel, P., Pelletier, S., Burgula, S., & Kanneganti, T.-D. (2020). Innate immune priming in the absence of TAK1 drives RIPK1 kinase activity–independent pyroptosis, apoptosis, necroptosis, and inflammatory disease. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20191644
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