Fas-independent T-cell apoptosis by dendritic cells controls autoimmune arthritis in MRL/lpr mice.

ABSTRACT:

Background

Although autoimmunity in MRL/lpr mice occurs due to a defect in Fas-mediated cell death of T cells, the role of Fas-independent apoptosis in pathogenesis has rarely been investigated. We have recently reported that receptor activator of nuclear factor (NF)-κB ligand (RANKL)-activated dendritic cells (DCs) play a key role in the pathogenesis of rheumatoid arthritis (RA) in MRL/lpr mice. We here attempted to establish a new therapeutic strategy with RANKL-activated DCs in RA by controlling apoptosis of peripheral T cells. Repeated transfer of RANKL-activated DCs into MRL/lpr mice was tested to determine whether this had a therapeutic effect on autoimmunity.

Methods and finding

Cellular and molecular mechanisms of Fas-independent apoptosis of T cells induced by the D

SUBMITTER: Izawa T 

PROVIDER: S-EPMC3523790 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature