0000000000165556
AUTHOR
Patrick S. Asmawidjaja
Dendritic Cell-Specific Deletion of β-Catenin Results in Fewer Regulatory T-Cells without Exacerbating Autoimmune Collagen-Induced Arthritis.
Dendritic cells (DCs) are professional antigen presenting cells that have the dual ability to stimulate immunity and maintain tolerance. However, the signalling pathways mediating tolerogenic DC function in vivo remain largely unknown. The beta-catenin pathway has been suggested to promote a regulatory DC phenotype. The aim of this study was to unravel the role of beta-catenin signalling to control DC function in the autoimmune collagen-induced arthritis model (CIA). Deletion of beta-catenin specifically in DCs was achieved by crossing conditional knockout mice with a CD11c-Cre transgenic mouse line. Bone marrow-derived DCs (BMDCs) were generated and used to study the maturation profile of …
A2.34 Specific deletion of β-catenin signalling in dendritic cells results in lower Treg expression without influencing the severity of collagen-induced arthritis
Background and objectives Rheumatoid arthritis (RA) is an autoimmune disease characterised by chronic inflammation and synovial infiltration of immune cells. T-cell priming by activated dendritic cells (DCs) contributes to the pathogenesis of RA. DCs are professional antigen presenting cells that have the dual ability to stimulate immunity and maintain tolerance. However, the signalling pathways mediating the tolerogenic DC function in vivo remain largely unknown. Recently, the b-catenin pathway has been suggested to promote a regulatory DC phenotype in vitro . While activation of β-catenin causes the phenotypic maturation of bone marrow-derived DCs, these cells fail to produce immunogenic …