FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3173681446> ?p ?o ?g. }

• W3173681446 abstract "Abstract Background Experimental autoimmune encephalomyelitis (EAE) is an animal disease model of multiple sclerosis (MS) that involves the immune system and central nervous system (CNS). However, it is unclear how genetic predispositions promote neuroinflammation in MS and EAE. Here, we investigated how partial loss-of-function of suppressor of MEK1 (SMEK1), a regulatory subunit of protein phosphatase 4, facilitates the onset of MS and EAE. Methods C57BL/6 mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG 35-55 ) to establish the EAE model. Clinical signs were recorded and pathogenesis was investigated after immunization. CNS tissues were analyzed by immunostaining, quantitative polymerase chain reaction (qPCR), western blot analysis, and enzyme-linked immunosorbent assay (ELISA). Single-cell analysis was carried out in the cortices and hippocampus. Splenic and lymph node cells were evaluated with flow cytometry, qPCR, and western blot analysis. Results Here, we showed that partial Smek1 deficiency caused more severe symptoms in the EAE model than in controls by activating myeloid cells and that Smek1 was required for maintaining immunosuppressive function by modulating the indoleamine 2,3-dioxygenase (IDO1)-aryl hydrocarbon receptor (AhR) pathway. Single-cell sequencing and an in vitro study showed that Smek1-deficient microglia and macrophages were preactivated at steady state. After MOG 35-55 immunization, microglia and macrophages underwent hyperactivation and produced increased IL-1β in Smek1 -/+ mice at the peak stage. Moreover, dysfunction of the IDO1-AhR pathway resulted from the reduction of interferon γ (IFN-γ), enhanced antigen presentation ability, and inhibition of anti-inflammatory processes in Smek1 -/+ EAE mice. Conclusions The present study suggests a protective role of Smek1 in autoimmune demyelination pathogenesis via immune suppression and inflammation regulation in both the immune system and the central nervous system. Our findings provide an instructive basis for the roles of Smek1 in EAE and broaden the understanding of the genetic factors involved in the pathogenesis of autoimmune demyelination." @default.
• W3173681446 created "2021-07-05" @default.
• W3173681446 creator A5001459715 @default.
• W3173681446 creator A5002457476 @default.
• W3173681446 creator A5018616023 @default.
• W3173681446 creator A5021905916 @default.
• W3173681446 creator A5029424603 @default.
• W3173681446 creator A5040622467 @default.
• W3173681446 creator A5041351751 @default.
• W3173681446 creator A5043843491 @default.
• W3173681446 creator A5067654292 @default.
• W3173681446 creator A5073878229 @default.
• W3173681446 date "2021-06-28" @default.
• W3173681446 modified "2023-09-23" @default.
• W3173681446 title "Smek1 deficiency exacerbates experimental autoimmune encephalomyelitis by activating proinflammatory microglia and suppressing the IDO1-AhR pathway" @default.
• W3173681446 cites W1510193398 @default.
• W3173681446 cites W1867019379 @default.
• W3173681446 cites W1922214571 @default.
• W3173681446 cites W1992021421 @default.
• W3173681446 cites W1992077904 @default.
• W3173681446 cites W1998142996 @default.
• W3173681446 cites W2001310133 @default.
• W3173681446 cites W2017006890 @default.
• W3173681446 cites W2024140382 @default.
• W3173681446 cites W2042400521 @default.
• W3173681446 cites W2052006922 @default.
• W3173681446 cites W2068712775 @default.
• W3173681446 cites W2075940342 @default.
• W3173681446 cites W2086080135 @default.
• W3173681446 cites W2099478515 @default.
• W3173681446 cites W2099840327 @default.
• W3173681446 cites W2113397738 @default.
• W3173681446 cites W2121758615 @default.
• W3173681446 cites W2135903996 @default.
• W3173681446 cites W2137988168 @default.
• W3173681446 cites W2138696766 @default.
• W3173681446 cites W2142177598 @default.
• W3173681446 cites W2147062889 @default.
• W3173681446 cites W2152857351 @default.
• W3173681446 cites W2162226607 @default.
• W3173681446 cites W2166378755 @default.
• W3173681446 cites W2299038626 @default.
• W3173681446 cites W2552680227 @default.
• W3173681446 cites W2558246554 @default.
• W3173681446 cites W2571287694 @default.
• W3173681446 cites W2610723541 @default.
• W3173681446 cites W2619332462 @default.
• W3173681446 cites W2620266814 @default.
• W3173681446 cites W2769228139 @default.
• W3173681446 cites W2795742782 @default.
• W3173681446 cites W2801908855 @default.
• W3173681446 cites W2888639178 @default.
• W3173681446 cites W2912181843 @default.
• W3173681446 cites W2921234203 @default.
• W3173681446 cites W2965238134 @default.
• W3173681446 cites W2966585750 @default.
• W3173681446 cites W2971337283 @default.
• W3173681446 cites W2980912316 @default.
• W3173681446 cites W2987137992 @default.
• W3173681446 cites W2998493548 @default.
• W3173681446 cites W2999155348 @default.
• W3173681446 cites W3009723063 @default.
• W3173681446 cites W3035612107 @default.
• W3173681446 cites W3112622226 @default.
• W3173681446 cites W47940757 @default.
• W3173681446 doi "https://doi.org/10.1186/s12974-021-02193-0" @default.
• W3173681446 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8237434" @default.
• W3173681446 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34183017" @default.
• W3173681446 hasPublicationYear "2021" @default.
• W3173681446 type Work @default.
• W3173681446 sameAs 3173681446 @default.
• W3173681446 citedByCount "6" @default.
• W3173681446 countsByYear W31736814462022 @default.
• W3173681446 countsByYear W31736814462023 @default.
• W3173681446 crossrefType "journal-article" @default.
• W3173681446 hasAuthorship W3173681446A5001459715 @default.
• W3173681446 hasAuthorship W3173681446A5002457476 @default.
• W3173681446 hasAuthorship W3173681446A5018616023 @default.
• W3173681446 hasAuthorship W3173681446A5021905916 @default.
• W3173681446 hasAuthorship W3173681446A5029424603 @default.
• W3173681446 hasAuthorship W3173681446A5040622467 @default.
• W3173681446 hasAuthorship W3173681446A5041351751 @default.
• W3173681446 hasAuthorship W3173681446A5043843491 @default.
• W3173681446 hasAuthorship W3173681446A5067654292 @default.
• W3173681446 hasAuthorship W3173681446A5073878229 @default.
• W3173681446 hasBestOaLocation W31736814461 @default.
• W3173681446 hasConcept C159654299 @default.
• W3173681446 hasConcept C163764329 @default.
• W3173681446 hasConcept C164027704 @default.
• W3173681446 hasConcept C203014093 @default.
• W3173681446 hasConcept C2776914184 @default.
• W3173681446 hasConcept C2777899865 @default.
• W3173681446 hasConcept C2778486448 @default.
• W3173681446 hasConcept C2779357208 @default.
• W3173681446 hasConcept C2779830541 @default.
• W3173681446 hasConcept C2780640218 @default.
• W3173681446 hasConcept C2781460105 @default.
• W3173681446 hasConcept C71924100 @default.
• W3173681446 hasConcept C86803240 @default.
• W3173681446 hasConcept C87753298 @default.

• next