Anti-citrullinated protein antibodies (ACPAs) are autoantibodies commonly observed in patients with rheumatoid arthritis (RA). Currently, most of the mechanisms of ACPA formation and bone destruction are well-understood, however, some unknown mechanisms still exist. There have been many new advances in ACPA-related clinical applications and targeted therapies. However, the existence of different ACPA subtypes is a limitation of targeted therapy. Herein, we present an overview of the process of ACPA generation, the underlying pathogenesis, and relevant clinical application and prospects.
Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thrombotic or obstetric events caused by persistent antiphospholipid antibodies (aPLs), namely lupus anticoagulant, anticardiolipin antibodies, or anti-b2 glycoprotein I (anti-b2GPI) antibodies. [1] The main target antigen in APS is b2GPI, through which aPL binds to the cell membrane and subsequently activates membrane receptors and downstream signal transducers. This may activate natural killer (NK) cells, leading to obstetric complications.
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