Characterization of the anticollagen antibody response in a new model of chronic polyarthritis.

OBJECTIVE: Type II collagen (CII)-specific B cell responses have been recognized in human rheumatoid arthritis (RA) and in collagen-induced arthritis (CIA). An important limitation of the CIA model is that the CII response and the disease are stimulated by exogenously injected collagen. A model of experimental ovalbumin (OVA)-mediated acute arthritis has been established in which autoimmunity is spontaneous and elicited by antigen-specific T cells. This study was undertaken to create a new model of chronic autoimmune polyarthritis and characterize the associated CII-specific B cell response. METHODS: Secondary challenge with OVA or CII in adjuvant was used to elicit chronic disease. CII-specific B cell responses against the epitopes U1, J1, C1, and citrullinated C1, together with the antibody affinity, were investigated in OVA-mediated arthritis. RESULTS: Chronic autoimmune polyarthritis was induced and was dependent on the antigen used in the secondary challenge. U1 was the major CII epitope recognized, and antibodies showed the same affinity as those in CIA. CONCLUSION: Our findings indicate that the development and severity of chronic disease is dependent on the antigen and is associated with an increased autoreactive B cell response directed against a specific CII epitope (U1). OVA-mediated chronic arthritis exhibits anti-CII antibodies (against U1), resembling human RA and murine CIA.