Sp3 ameliorated experimental autoimmune encephalomyelitis by triggering Socs3 in Th17 cells.

ABSTRACT:

Introduction

Although it is believed that chronic inflammatory and degenerative diseases of the central nervous system are mediated by autoimmune Th17 cells, the underlying mechanisms remain largely unexplored. Recent studies and our research have revealed that Sp3 was blocked in multiple sclerosis (MS) patients and experimental autoimmune encephalomyelitis (EAE). However, it remained unclear why it is silent and how it regulates Th17 cell differentiation in MS.

Objectives

This study aimed to explore the impact of Sp3 on Th17 cell-mediated EAE and the underlying mechanism.

Methods

The effect of Sp3 on the clinical symptoms of EAE was evaluated by scoring, histochemistry, and fast blue (FB) techniques, scRNA-seq data analysis, flow cytometry, ELISA, PCR, WB, immunofluo

SUBMITTER: Li Y 

PROVIDER: S-EPMC12684914 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature