{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Patton T"],"funding":["Department of Health | National Health and Medical Research Council (NHMRC)"],"pagination":["111"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9922319"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(2)"],"pubmed_abstract":["Cell death mechanisms in T lymphocytes vary according to their developmental stage, cell subset and activation status. The cell death control mechanisms of mucosal-associated invariant T (MAIT) cells, a specialized T cell population, are largely unknown. Here we report that MAIT cells express key necroptotic machinery; receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) protein, in abundance. Despite this, we discovered that the loss of RIPK3, but not necroptotic effector MLKL or apoptotic caspase-8, specifically increased MAIT cell abundance at steady-state in the thymus, spleen, liver and lungs, in a cell-intrinsic manner. In contrast, over the course of infection with Francisella tularensis, RIPK3 deficiency did not impact the magnitude of the expan"],"journal":["Cell death & disease"],"pubmed_title":["RIPK3 controls MAIT cell accumulation during development but not during infection."],"pmcid":["PMC9922319"],"funding_grant_id":["1120467","1145788","1113293","1193745","1105209","1196881"],"pubmed_authors":["Zhang JG","Pediongco TJ","Patton T","Koay HF","Jacquelot N","Lawlor KE","Wang H","Zhao Z","McCluskey J","Zhan Y","Ennis B","Nelson AG","Djajawi TM","Eckle SBG","Chen Z","Eddy E","Lew AM","Louis C","Lim XY","Lalaoui N","Souter MNT","Pellicci DG","Corbett AJ"],"additional_accession":[]},"is_claimable":false,"name":"RIPK3 controls MAIT cell accumulation during development but not during infection.","description":"Cell death mechanisms in T lymphocytes vary according to their developmental stage, cell subset and activation status. The cell death control mechanisms of mucosal-associated invariant T (MAIT) cells, a specialized T cell population, are largely unknown. Here we report that MAIT cells express key necroptotic machinery; receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) protein, in abundance. Despite this, we discovered that the loss of RIPK3, but not necroptotic effector MLKL or apoptotic caspase-8, specifically increased MAIT cell abundance at steady-state in the thymus, spleen, liver and lungs, in a cell-intrinsic manner. In contrast, over the course of infection with Francisella tularensis, RIPK3 deficiency did not impact the magnitude of the expan","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2025-04-18T20:04:24.937Z","creation":"2025-04-07T07:50:43.545Z"},"accession":"S-EPMC9922319","cross_references":{"pubmed":["36774342"],"doi":["10.1038/s41419-023-05619-0"]}}