A01 - Mechanisms of cell death-induced inflammation
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Manolis Pasparakis
Institute for genetics, CECAD, University of Cologne
Contact: pasparakis(at)uni-koeln.de
For more information visit: Pasparakis lab
Abstract
Studies in mouse models provided evidence that cell death triggers inflammation, however the underlying mechanisms remain elusive. Using relevant genetic mouse models, this project will study the mechanisms by which different types of cell death trigger inflammation in vivo, focusing primarily on apoptosis and necroptosis. Major focus areas will be the in vivo role of specific DAMPs and their receptors as well as the mechanisms determining DAMP release via plasma membrane permeabilisation and their functional consequences in triggering cell death-induced inflammation.
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Recent Publications
Koerner L, Wachsmuth L, Kumari S, Schwarzer R, Wagner T, Jiao H, Pasparakis M. ZBP1 causes inflammation by inducing RIPK3-mediated necroptosis and RIPK1 kinase activity-independent apoptosis. Cell Death Differ. 2024 Jun 7. doi: 10.1038/s41418-024-01321-6. Epub ahead of print. PMID: 38849574.
Imai T, Lin J, Kaya G, Ju E, Kondylis V, Kelepouras K, Liccardi G, Kim C, Pasparakis M. 1,2,4. The RIPK1 death domain restrains ZBP1- and TRIF-mediated cell death and inflammation. Immunity 57, 1–17, https://doi.org/10.1016/j.immuni.2024.04.016
Eren, R.O., Kaya, G.G., Schwarzer, R. and Pasparakis, M. (2024). IKKε and TBK1 prevent RIPK1 dependent and independent inflammation. Nat Commun. 15, 130. doi: 10.1038/s41467-023-44372-y.