PAD2 deficiency in mice reduced anti-collagen antibody levels in collagen-induced arthritis and impaired persistent hemagglutination inhibiting antibodies and protection from lethal influenza.
PAD2 plays a modest but significant role in both normal antiviral antibody responses and abnormal autoantibody responses in inflammatory arthritis.
The peptidylarginine deiminases (PADs) and the citrullinated proteins that they generate have key roles in innate immunity and rheumatoid arthritis, an inflammatory arthritis with antibodies that target citrullinated proteins. However, the importance of PADs, particularly PAD2, in the adaptive immune response, both normal and pathogenic, is newly emerging. In this study, we evaluated a requirement for PAD2 in the antibody response in collagen-induced arthritis (CIA), a T and B cell-driven murine model of rheumatoid arthritis, and in the protective antibody response to murine influenza infection. Using PAD2-/- and PAD2+/+ mice on the DBA/1J background, we found that PAD2 is required for maximal anti-collagen antibody levels, but not collagen-specific plasma cell numbers, T cell activation or polarization, or arthritis severity in CIA. Also, we found that PAD2 is required not just for normal levels of persistent hemagglutination inhibiting antibodies but also for full protection from lethal influenza rechallenge. Together, these data provide evidence for a novel modest requirement for PAD2 in a normal antiviral antibody response and in an abnormal autoantibody response in inflammatory arthritis.
Mergaert et al. (Mon,) conducted a other in Collagen-induced arthritis and influenza infection. PAD2 deficiency (PAD2-/-) vs. PAD2+/+ mice was evaluated on Anti-collagen antibody levels, arthritis severity, hemagglutination inhibiting antibodies, and protection from lethal influenza rechallenge. PAD2 deficiency in mice reduced anti-collagen antibody levels in collagen-induced arthritis and impaired persistent hemagglutination inhibiting antibodies and protection from lethal influenza.