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• W2927917099 abstract "Dysregulation of the JAK/STAT signaling pathway is associated with multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE). Suppressors of cytokine signaling (SOCS) negatively regulate the JAK/STAT pathway. We previously reported a severe, brain-targeted, atypical form of EAE in mice lacking Socs3 in myeloid cells (Socs3ΔLysM), and that this atypical EAE is associated with cerebellar neutrophil infiltration. There is emerging evidence that neutrophils are detrimental in the pathology of MS/EAE; however, their exact function is unclear. Here we demonstrate that neutrophils from the cerebellum of Socs3ΔLysM mice show a hyperactivated phenotype with excessive production of reactive oxygen species (ROS) at the peak of EAE. Neutralization of ROS in vivo delayed the onset and reduced severity of atypical EAE. Mechanistically, Socs3-deficient neutrophils exhibited enhanced signal transducer and activator of transcription 3 (STAT3) activation, a hyperactivated phenotype in response to granulocyte colony–stimulating factor (G-CSF), and upon G-CSF priming, increased ROS production. Neutralization of G-CSF in vivo significantly reduced the incidence and severity of the atypical EAE phenotype. Overall, our work elucidates that hypersensitivity of G-CSF/STAT3 signaling in Socs3ΔLysM mice leads to atypical EAE by enhanced neutrophil activation and increased oxidative stress, which may explain the detrimental role of G-CSF in MS patients." @default.
• W2927917099 created "2019-04-11" @default.
• W2927917099 creator A5005357486 @default.
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• W2927917099 date "2019-05-02" @default.
• W2927917099 modified "2023-10-14" @default.
• W2927917099 title "Deficiency of Socs3 leads to brain-targeted experimental autoimmune encephalomyelitis via enhanced neutrophil activation and ROS production" @default.
• W2927917099 cites W1483410121 @default.
• W2927917099 cites W1519204637 @default.
• W2927917099 cites W1523338791 @default.
• W2927917099 cites W1526060303 @default.
• W2927917099 cites W1629107208 @default.
• W2927917099 cites W1644741425 @default.
• W2927917099 cites W1828576284 @default.
• W2927917099 cites W1905660905 @default.
• W2927917099 cites W1937954415 @default.
• W2927917099 cites W1945944294 @default.
• W2927917099 cites W1957500455 @default.
• W2927917099 cites W1972467243 @default.
• W2927917099 cites W1978816877 @default.
• W2927917099 cites W1991019975 @default.
• W2927917099 cites W1997090182 @default.
• W2927917099 cites W2004638361 @default.
• W2927917099 cites W2009454655 @default.
• W2927917099 cites W2011044675 @default.
• W2927917099 cites W2011190955 @default.
• W2927917099 cites W2017437933 @default.
• W2927917099 cites W2030726748 @default.
• W2927917099 cites W2033753616 @default.
• W2927917099 cites W2037265282 @default.
• W2927917099 cites W2038445887 @default.
• W2927917099 cites W2040551905 @default.
• W2927917099 cites W2041168245 @default.
• W2927917099 cites W2051609779 @default.
• W2927917099 cites W2056505450 @default.
• W2927917099 cites W207029473 @default.
• W2927917099 cites W2071886519 @default.
• W2927917099 cites W2073387289 @default.
• W2927917099 cites W2076794463 @default.
• W2927917099 cites W2083218881 @default.
• W2927917099 cites W2086971705 @default.
• W2927917099 cites W2090106964 @default.
• W2927917099 cites W2096584676 @default.
• W2927917099 cites W2097780447 @default.
• W2927917099 cites W2098308289 @default.
• W2927917099 cites W2098613848 @default.
• W2927917099 cites W2103659606 @default.
• W2927917099 cites W2110299641 @default.
• W2927917099 cites W2112671019 @default.
• W2927917099 cites W2112884134 @default.
• W2927917099 cites W2120307001 @default.
• W2927917099 cites W2128597204 @default.
• W2927917099 cites W2129229339 @default.
• W2927917099 cites W2132173287 @default.
• W2927917099 cites W2136266325 @default.
• W2927917099 cites W2139181115 @default.
• W2927917099 cites W2140013858 @default.
• W2927917099 cites W2147495692 @default.
• W2927917099 cites W2157837362 @default.
• W2927917099 cites W2161948816 @default.
• W2927917099 cites W2162981836 @default.
• W2927917099 cites W2166716152 @default.
• W2927917099 cites W2168436315 @default.
• W2927917099 cites W2169798952 @default.
• W2927917099 cites W2171318929 @default.
• W2927917099 cites W2176490156 @default.
• W2927917099 cites W2182323848 @default.
• W2927917099 cites W2210729715 @default.
• W2927917099 cites W2260668364 @default.
• W2927917099 cites W2272972580 @default.
• W2927917099 cites W2284327277 @default.
• W2927917099 cites W2296407400 @default.
• W2927917099 cites W2309813174 @default.
• W2927917099 cites W2317865868 @default.
• W2927917099 cites W2346793309 @default.
• W2927917099 cites W2463277633 @default.
• W2927917099 cites W2486481384 @default.
• W2927917099 cites W2491054150 @default.
• W2927917099 cites W2502558265 @default.
• W2927917099 cites W2528968729 @default.
• W2927917099 cites W2548228770 @default.
• W2927917099 cites W2551685001 @default.
• W2927917099 cites W2578607799 @default.
• W2927917099 cites W2584421506 @default.
• W2927917099 cites W2589256120 @default.
• W2927917099 cites W2596984373 @default.
• W2927917099 cites W2601742683 @default.
• W2927917099 cites W2604511302 @default.
• W2927917099 cites W2605171403 @default.
• W2927917099 cites W2614085156 @default.

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