Induction of chronic destructive arthritis in SCID mice by arthritogenic fibroblast-like synoviocytes derived from mice with antigen-induced arthritis

Fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA) are autonomously activated to maintain inflammation and joint destruction in co-transplantation models. To elucidate inducing mechanisms involved in this altered behavior, the arthritogenic potential of FLSs from murine...

Full description

Saved in:
Bibliographic Details
Published in:Arthritis research & therapy 2018-11, Vol.20 (1), p.261-261, Article 261
Main Authors: Frey, Oliver, Hückel, Marion, Gajda, Mieczyslaw, Petrow, Peter K, Bräuer, Rolf
Format: Article
Language:English
Subjects:
Animals
Antigens
Arthritis
Care and treatment
Chemokines
Cytokines
Development and progression
Fibroblasts
Immune system
Inflammation
Joint destruction
Medical examination
Medical research
Pathogenesis
Peptides
Rheumatoid arthritis
Rodents
Synovial fibroblast
Synovial membrane
Tumor necrosis factor-TNF
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA) are autonomously activated to maintain inflammation and joint destruction in co-transplantation models. To elucidate inducing mechanisms involved in this altered behavior, the arthritogenic potential of FLSs from murine antigen-induced arthritis (AIA) were investigated in a transfer model. FLSs were isolated, expanded in vitro, and transferred into knee joint cavities of severe combined immunodeficient (SCID) mice. Their arthritogenic capacity was assessed by monitoring joint swelling and evaluation of histological parameters 70 to 100 days after transfer. FLSs from AIA mice were able to transfer arthritis into recipient SCID mice. FLS transfer induced a chronic arthritis with recruitment of inflammatory cells and marked cartilage destruction. Long-lasting inflammation was not required for imprinting of arthritogenicity in FLSs since cells isolated from acute arthritic joints were fully competent to transfer arthritis. We also observed arthritogenic potential in FLSs isolated from contralateral non-arthritic joints in our monoarticular arthritis model. We show that the transformation of FLSs into arthritogenic cells occurs early in arthritis development. This challenges current hypotheses on the role of these cells in arthritis pathogenesis and opens up the way for further mechanistic studies.
ISSN:1478-6362
1478-6354
1478-6362
DOI:10.1186/s13075-018-1720-y