B cell depletion in early rheumatoid arthritis: a new concept in therapeutics. Anti-CCP antibodies: the past, the present and the future. Characterization of the antibody response in mice with type II collagen-induced arthritis, using monoclonal anti-type II collagen antibodies. Holmdahl, R., Rubin, K., Klareskog, L., Larsson, E. Arthritis provoked by linked T and B cell recognition of a glycolytic enzyme. B cell-deficient mice do not develop type II collagen-induced arthritis (CIA).
Induction and suppression of collagen-induced arthritis is dependent on distinct Fcγ receptors. Essential role for the C5a receptor in regulating the effector phase of synovial infiltration and joint destruction in experimental arthritis. Arthritis critically dependent on innate immune system players. The pathogenesis of rheumatoid arthritis. Asymptomatic humans with rheumatoid arthritis (RA)-specific autoantibodies showed identical changes in the activity and glycosylation of autoreactive IgG antibodies before shifting to the inflammatory phase of RA thus, our results identify an IL-23–T H17 cell–dependent pathway that controls autoantibody activity and unmasks a preexisting breach in immunotolerance. By instructing B cells in an IL-22- and IL-21-dependent manner, T H17 cells regulated the expression of β-galactoside α2,6-sialyltransferase 1 in newly differentiating antibody-producing cells and determined the glycosylation profile and activity of immunoglobulin G (IgG) produced by the plasma cells that subsequently emerged. Here we identified the axis of interleukin 23 (IL-23) and the T H17 subset of helper T cells as a decisive factor that controlled the intrinsic inflammatory activity of autoantibodies and triggered the clinical onset of autoimmune arthritis. The checkpoints and mechanisms that contribute to autoantibody-driven disease are as yet incompletely understood. Nature Immunology volume 18, pages 104–113 ( 2017) Cite this article
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