Email updates

Keep up to date with the latest news and content from Arthritis Research & Therapy and BioMed Central.

Open Access Research article

Bystander suppression of collagen-induced arthritis in mice fed ovalbumin

N Fredrik Bäckström1* and Ulf IH Dahlgren12

Author Affiliations

1 Faculty of Odontology, Section of Oral Immunology, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden

2 Department of Rheumatology and Inflammation Research, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden

For all author emails, please log on.

Arthritis Res Ther 2004, 6:R151-R160  doi:10.1186/ar1150

Published: 5 February 2004

Abstract

We wanted to assess whether B-cell and/or T-cell responses to collagen and thereby the course of collagen-induced arthritis could be suppressed by regulatory mechanisms associated with oral tolerance to an unrelated protein. DBA/1 mice were fed ovalbumin (OVA)-containing pellets ad libitum for 1 week and subsequently coimmunized twice, with a mixture of bovine collagen type II (BCII) and OVA in Freund's complete adjuvant. Mice fed OVA before coimmunization with BCII and OVA had significantly lower arthritic scores than mice immunized with BCII only. Their body weight increased during the study period and their anti-BCII antibody activity was significantly IgG2a lower. The frequency of spleen cells producing IgG anti-BCII antibody was also reduced. Coimmunization per se slightly ameliorated the development of arthritis, resulting in an early, transient reduction. It resulted in significantly higher IgG1 anti-BCII antibody activity and increased splenocyte secretion of IFN-γ and IL-10 in response to BCII. Our findings demonstrate that OVA-specific regulatory events induced by feeding OVA, i.e. bystander suppression, reduced the severity of arthritis in animals immunized with BCII and OVA. Anti-BCII specific antibody responses and cytokine secretion by types 1 and 2 T helper cells were also decreased.

Keywords:
bystander suppression; collagen-induced arthritis; mice; oral tolerance; Th1/Th2 cells