Overexpression of the ubiquitin-editing enzyme A20 in the brain lesions of Multiple Sclerosis patients: moving from systemic to central nervous system inflammation.

ABSTRACT: Multiple Sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS) in which inflammation plays a key pathological role. Recent evidences showed that systemic inflammation induces increasing cell infiltration within meninges and perivascular spaces in the brain parenchyma, triggering resident microglial and astrocytic activation. The anti-inflammatory enzyme A20, also named TNF associated protein 3 (TNFAIP3), is considered a central gatekeeper in inflammation and peripheral immune system regulation through the inhibition of NF-kB. The TNFAIP3 locus is genetically associated to MS and its transcripts is downregulated in blood cells in treatment-naïve MS patients. Recently, several evidences in mouse models have led to hypothesize a function of A20 also in the CNS.

SUBMITTER: Perga S 

PROVIDER: S-EPMC8018032 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature