dc.date.accessioned | 2023-02-22T19:19:22Z | |
dc.date.available | 2023-02-22T19:19:22Z | |
dc.date.created | 2022-11-23T10:27:34Z | |
dc.date.issued | 2022 | |
dc.identifier.citation | Mehto, Subhash Jena, Kautilya Kumar Yadav, Rina Priyadarsini, Swatismita Samal, Pallavi Krishna, Sivaram Dhar, Kollori Jain, Ashish Chauhan, Nishant Ranjan Murmu, Krushna C Bal, Ramyasingh Sahu, Rinku Jaiswal, Pundrik Sahoo, Bhabani Sankar Patnaik, Srinivas Kufer, Thomas A Rusten, Tor Erik Chauhan, Swati Prasad, Punit Chauhan, Santosh . Selective autophagy of RIPosomes maintains innate immune homeostasis during bacterial infection. EMBO Journal. 2022, 1-23 | |
dc.identifier.uri | http://hdl.handle.net/10852/100388 | |
dc.description.abstract | The NOD1/2-RIPK2 is a key cytosolic signaling complex that activates NF-κB pro-inflammatory response against invading pathogens. However, uncontrolled NF-κB signaling can cause tissue damage leading to chronic diseases. The mechanisms by which the NODs-RIPK2-NF-κB innate immune axis is activated and resolved remain poorly understood. Here, we demonstrate that bacterial infection induces the formation of endogenous RIPK2 oligomers (RIPosomes) that are self-assembling entities that coat the bacteria to induce NF-κB response. Next, we show that autophagy proteins IRGM and p62/SQSTM1 physically interact with NOD1/2, RIPK2 and RIPosomes to promote their selective autophagy and limit NF-κB activation. IRGM suppresses RIPK2-dependent pro-inflammatory programs induced by Shigella and Salmonella. Consistently, the therapeutic inhibition of RIPK2 ameliorates Shigella infection- and DSS-induced gut inflammation in Irgm1 KO mice. This study identifies a unique mechanism where the innate immune proteins and autophagy machinery are recruited together to the bacteria for defense as well as for maintaining immune homeostasis. | |
dc.language | EN | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.title | Selective autophagy of RIPosomes maintains innate immune homeostasis during bacterial infection | |
dc.title.alternative | ENEngelskEnglishSelective autophagy of RIPosomes maintains innate immune homeostasis during bacterial infection | |
dc.type | Journal article | |
dc.creator.author | Mehto, Subhash | |
dc.creator.author | Jena, Kautilya Kumar | |
dc.creator.author | Yadav, Rina | |
dc.creator.author | Priyadarsini, Swatismita | |
dc.creator.author | Samal, Pallavi | |
dc.creator.author | Krishna, Sivaram | |
dc.creator.author | Dhar, Kollori | |
dc.creator.author | Jain, Ashish | |
dc.creator.author | Chauhan, Nishant Ranjan | |
dc.creator.author | Murmu, Krushna C | |
dc.creator.author | Bal, Ramyasingh | |
dc.creator.author | Sahu, Rinku | |
dc.creator.author | Jaiswal, Pundrik | |
dc.creator.author | Sahoo, Bhabani Sankar | |
dc.creator.author | Patnaik, Srinivas | |
dc.creator.author | Kufer, Thomas A | |
dc.creator.author | Rusten, Tor Erik | |
dc.creator.author | Chauhan, Swati | |
dc.creator.author | Prasad, Punit | |
dc.creator.author | Chauhan, Santosh | |
cristin.unitcode | 185,53,2,15 | |
cristin.unitname | Senter for kreftcelle-reprogrammering | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 2 | |
dc.identifier.cristin | 2078973 | |
dc.identifier.bibliographiccitation | info:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=EMBO Journal&rft.volume=&rft.spage=1&rft.date=2022 | |
dc.identifier.jtitle | EMBO Journal | |
dc.identifier.volume | 41 | |
dc.identifier.endpage | 23 | |
dc.identifier.doi | https://doi.org/10.15252/embj.2022111289 | |
dc.type.document | Tidsskriftartikkel | |
dc.type.peerreviewed | Peer reviewed | |
dc.source.issn | 0261-4189 | |
dc.type.version | PublishedVersion | |
cristin.articleid | e111289 | |