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Intravenous immunoglobulin ( IVIG ) is widely used in autoimmune neuromuscular diseases whose pathogenesis is undefined. Many different effects of  IVIG  have been demonstrated  in vitro , but few studies actually identify the mechanism(s) most important  in vivo . Doses and treatment intervals are generally chosen empirically. Recent studies in Guillain‐Barré syndrome and chronic inflammatory demyelinating polyneuropathy show that some effects of  IVIG  are readily reversible and highly dependent on the serum  IgG  level. This suggests that in some autoantibody‐mediated neuromuscular diseases,  IVIG  directly competes with autoantibodies that reversibly interfere with nerve conduction. Mechanisms of action of  IVIG  which most likely involve direct competition with autoantibodies include: neutralization of autoantibodies by anti‐idiotypes, inhibition of complement deposition, and increasing catabolism of pathologic antibodies by saturating  FcRn . Indirect immunomodulatory effects are not as likely to involve competition and may not have the same reversibility and dose‐dependency. Pharmacodynamic analyses should be informative regarding most relevant mechanism(s) of action of  IVIG  as well as the role of autoantibodies in the immunopathogenesis of each disease. Better understanding of the role of autoantibodies and of the target(s) of  IVIG  could lead to more efficient use of this therapy and better patient outcomes.

journal of the peripheral nervous system

Rapid and reversible responses to  IVIG  in autoimmune neuromuscular diseases suggest mechanisms of action involving competition with functionally important autoantibodies