Anti-CarP antibodies stabilize carH3 within NETs, amplifying its pro-inflammatory and osteoclastogenic activity. The resulting carH3-IgG ICs potently activate FLS, linking humoral immunity to tissue inflammation and bone destruction in RA. These findings identify carH3 stabilization as a potential therapeutic target in antibody-mediated joint damage.
Nakabo et al. (Fri,) studied this question.