ACPA response in evolution of rheumatoid arthritis

The ACPA response is different from conventional antibody responses. The ACPA response is generally of a much lower avidity than recall responses. Avidity maturation is limited and occurs before disease onset. The presence of low avidity ACPA is associated with higher rate of joint destruction. In vitro, the binding of low avidity ACPA to citrullinated epitopes was weakly inhibited by citrullinated antigens and low avidity ACPA have a higher ability to activate the complement system. In addition, there are certain antigens which continuously drive ACPA (IgM) response in RA.Ramathibodi hospital, Mahidol university, Bangkok, ThailandUBL - phd migration 201

Expression of the Inherently Autoreactive Idiotope 9G4 on Autoantibodies to Citrullinated Peptides and on Rheumatoid Factors in Patients with Early and Established Rheumatoid Arthritis.

The pre-symptomatic stage of Rheumatoid arthritis (RA) is associated with pro-inflammatory cytokines and autoantibodies. High levels and epitope spread by Rheumatoid factors (RhF) and autoantibodies to citrullinated proteins signify progression towards disease expression. In established RA, the persistence of high autoantibody levels reflects production by both long-lived plasma cells and short-lived plasmablasts. Neither the relative contributions to pathogenesis by autoantibodies from either source, nor the factors responsible for deciding the fate of autoantigen specific 'parent' B-cells, is understood. Phenotypic markers identifying subsets of autoreactive B-cells are therefore of interest in understanding the origin and perpetuation of the autoimmune response in RA. One such phenotypic marker is the rat monoclonal antibody, 9G4, which recognises an idiotope on immunoglobuins derived from the inherently autoreactive VH-gene, VH4-34. We therefore investigated whether the 9G4 idiotope was expressed on autoantibodies in patients with RA

ACPA response in evolution of rheumatoid arthritis

The ACPA response is different from conventional antibody responses. The ACPA response is generally of a much lower avidity than recall responses. Avidity maturation is limited and occurs before disease onset. The presence of low avidity ACPA is associated with higher rate of joint destruction. In vitro, the binding of low avidity ACPA to citrullinated epitopes was weakly inhibited by citrullinated antigens and low avidity ACPA have a higher ability to activate the complement system. In addition, there are certain antigens which continuously drive ACPA (IgM) response in RA

Anti-citrullinated protein antibodies (ACPA) in early rheumatoid arthritis

Pathophysiology and treatment of rheumatic disease

THE ACPA IGM FINE SPECIFICITY DIFFERS FROM THE ACPA IGG ANTIGEN-RECOGNITION PROFILE

Pathophysiology and treatment of rheumatic disease

Enhanced complement activation by low-avidity anti-citrullinated protein antibodies (ACPA) possibly explains the association with enhanced joint destruction in rheumatoid arthritis

Pathophysiology and treatment of rheumatic disease