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USP15 regulates type I interferon response and is...
Journal article

USP15 regulates type I interferon response and is required for pathogenesis of neuroinflammation

Abstract

Cerebral malaria infection can provoke fatal neuroinflammation. Gros and colleagues identify an ubiquitin-modification axis that exacerbates neuroinflammation and that involves TRIM25 and USP15, which jointly promote type I interferon production.

Authors

Torre S; Polyak MJ; Langlais D; Fodil N; Kennedy JM; Radovanovic I; Berghout J; Leiva-Torres GA; Krawczyk CM; Ilangumaran S

Journal

Nature Immunology, Vol. 18, No. 1, pp. 54–63

Publisher

Springer Nature

Publication Date

January 1, 2017

DOI

10.1038/ni.3581

ISSN

1529-2908

Associated Experts

Karen Mossman

Professor, Faculty of Health Sciences
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Labels

Fields of Research (FoR)

3207 Medical Microbiology32 Biomedical and Clinical Sciences3202 Clinical Sciences3101 Biochemistry and cell biology3204 Immunology

Sustainable Development Goals (SDG)

3 Good Health and Well Being

Medical Subject Headings (MeSH)

AnimalsDNA-Binding ProteinsEncephalomyelitis, Autoimmune, ExperimentalHEK293 CellsHumansImmunity, InnateInterferon Type IMalaria, CerebralMiceMice, 129 StrainMice, Inbred C57BLMice, TransgenicMolecular Targeted TherapyMyelin-Oligodendrocyte GlycoproteinNeurogenic InflammationPeptide FragmentsPlasmodium bergheiTranscription FactorsUbiquitin-Specific Proteases
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