STEAP4 expression in CNS resident cells promotes Th17 cell-induced autoimmune encephalomyelitis.

ABSTRACT:

Background

Multiple sclerosis (MS) is a debilitating neurological disease caused by autoimmune destruction of the myelin sheath. Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model for the pathogenesis of MS. We and others have previously demonstrated that IL-17 is critical for the pathogenesis of EAE. The concentration of IL-17 is significantly higher in the sera of MS patients than in healthy controls and correlates with disease activity. Moreover, anti-IL-17 neutralizing antibody demonstrated promising efficacy in a phase II trial in MS patients, further substantiating a key pathogenic role for IL-17 in MS. While Th17 and IL-17 are emerging as a bona fide drivers for neuroinflammation, it remains unclear what effector molecule executes the inflammatory

SUBMITTER: Zhao J 

PROVIDER: S-EPMC8059164 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature