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Loss of USP18 in microglia induces white matter pathology

Loss of USP18 in microglia induces white matter pathology

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_236b33d0bdba497fb77c847152b3950b

Loss of USP18 in microglia induces white matter pathology

About this item

Full title

Loss of USP18 in microglia induces white matter pathology

Publisher

England: BioMed Central Ltd

Journal title

Acta neuropathologica communications, 2019-07, Vol.7 (1), p.106-106, Article 106

Language

English

Formats

Publication information

Publisher

England: BioMed Central Ltd

More information

Scope and Contents

Contents

[...]experiments undertaken in mice demonstrate that overexpression of interferon in the CNS results in neuropathology reminiscent of that seen in certain type I interferonopathies [1, 10]. The escalating spiral of white matter damage might be initiated by type I IFN that is induced in microglia via stimulator of interferon genes (STING), and this IFN likely influences the microglial phenotype in an autocrine and paracrine fashion [13]. Akwa Y, Hassett DE, Eloranta ML, Sandberg K, Masliah E, Powell H, Whitton JL, Bloom FE, Campbell IL (1998) Transgenic expression of IFN-alpha in the central nervous system of mice protects against lethal neurotropic viral infection but induces inflammation and neurodegeneration. Cell Death Dis 7:e2444. https://doi.org/10.1038/cddis.2016.326 View ArticlePubMedPubMed CentralGoogle Scholar Kavanagh D, McGlasson S, Jury A, Williams J, Scolding N, Bellamy C, Gunther C, Ritchie D, Gale DP, Kanwar YS et al (2016) Type I interferon causes thrombotic microangiopathy by a dose-dependent toxic effect on the microvasculature....

Alternative Titles

Full title

Loss of USP18 in microglia induces white matter pathology

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Primary Identifiers

Record Identifier

TN_cdi_doaj_primary_oai_doaj_org_article_236b33d0bdba497fb77c847152b3950b

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_236b33d0bdba497fb77c847152b3950b

Other Identifiers

ISSN

2051-5960

E-ISSN

2051-5960

DOI

10.1186/s40478-019-0757-8

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