Therefore, restraining IgA IC binding to Fcα receptors, for instance by anti-CD89 antibodies or saturating CD89 with monomeric IgA, are potential therapeutic options to avoid triggering of arthritis.30 31 Also, since IgA glycosylation patterns have proved important for effector functions,32 increased IgA sialylation could hypothetically reduce progression to arthritis. Here, FCAR is linked to Arthritis.