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Tovey Crutchfield, Emma C; Garnish, Sarah E; Day, Jessica; Anderton, Holly; Chiou, Shene; Hempel, Anne; Hall, Cathrine; Patel, Komal M; Gangatirkar, Pradnya; Martin, Katherine R; Li Wai Suen, Connie S N; Garnham, Alexandra L; Kueh, Andrew J; Wicks, Ian P; Silke, John; Nachbur, Ueli; Samson, Andre L; Murphy, James M; Hildebrand, Joanne M
Cell death and differentiation, 04/2023, Letnik: 30, Številka: 4Journal Article
MLKL and RIPK3 are the core signaling proteins of the inflammatory cell death pathway, necroptosis, which is a known mediator and modifier of human disease. Necroptosis has been implicated in the progression of disease in almost every physiological system and recent reports suggest a role for necroptosis in aging. Here, we present the first comprehensive analysis of age-related histopathological and immunological phenotypes in a cohort of Mlkl and Ripk3 mice on a congenic C57BL/6 J genetic background. We show that genetic deletion of Mlkl in female mice interrupts immune system aging, specifically delaying the age-related reduction of circulating lymphocytes. -Seventeen-month-old Mlkl female mice were also protected against age-related chronic sterile inflammation in connective tissue and skeletal muscle relative to wild-type littermate controls, exhibiting a reduced number of immune cell infiltrates in these sites and fewer regenerating myocytes. These observations implicate MLKL in age-related sterile inflammation, suggesting a possible application for long-term anti-necroptotic therapy in humans.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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