Id2 exacerbates the development of rheumatoid arthritis by increasing IFN-γ production in CD4⁺ T cells.

ABSTRACT:

Purpose

This research investigates the role of inhibitor of differentiation 2 (Id2) in the synthesis of pro-inflammatory cytokines, specifically interferon-γ (IFN-γ) and interleukin-17 (IL-17), by various subsets of T cells, and its pathogenic role in rheumatoid arthritis (RA).

Methods

Flow cytometry was employed to assess T-cell activation and Id2 expression in 72 RA patients and 23 healthy controls. In vitro, peripheral blood mononuclear cells were treated with either an Id2 inhibitor or a T-cell co-stimulation inhibitor. An in vivo collagen-induced arthritis (CIA) model was established using T-cell-specific Id2 knockout mice. Additionally, follow-up observations were conducted among treated RA patients.

Results

T-cell activation levels in RA synovial fluid were sig

SUBMITTER: Sun H 

PROVIDER: S-EPMC11885165 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature