Differential Cytokine Changes in Patients with Myasthenia Gravis with Antibodies against AChR and MuSK.

Neuromuscular transmission failure in myasthenia gravis (MG) is most commonly elicited by autoantibodies (ab) to the acetylcholine receptor or the muscle-specific kinase, constituting AChR-MG and MuSK-MG. It is controversial whether these MG subtypes arise through different T helper (Th) 1, Th2 or Th17 polarized immune reactions and how these reactions are blunted by immunosuppression. To address these questions, plasma levels of cytokines related to various Th subtypes were determined in patients with AChR-MG, MuSK-MG and healthy controls (CON).

Antigen-specific apheresis of autoantibodies in myasthenia gravis.

Myasthenia gravis (MG) is an autoimmune disorder affecting the neuromuscular junction, usually caused by autoantibodies against the acetylcholine receptor (AChR) or the muscle-specific kinase (MuSK). Our aim is the development of a therapy based on the selective extracorporeal elimination of anti-AChR or anti-MuSK antibodies. To this end, the extracellular domains of the AChR subunits and MuSK have been expressed in yeast to be used as adsorbents, after optimization, and to obtain large quantities of proteins with near-native structure.