Experimental Therapies: What the Future May Have in Store
Henry J. Kaminski, M.D.
Chairman
Department of Neurology & Psychiatry
Saint Louis University
Myasthenia gravis is the best understood of all autoimmune disorders. The Figure below
illustrates the many steps that are involved in causing neuromuscular junction injury which is the
cause of weakness in patients with MG. Once the antibody binds the muscle a membrane attack
complex (MAC) is formed which is the end product of the normal complement system (C),
which normally protects humans from cancers and infections. The abnormal antibodies (AChRAb) are formed by B cells that regulated by T helper cells. These T cells and B cells are
activated by antigen presenting cells (APC) that have portions of proteins that look like parts of
the acetylcholine receptor (AChR). The cartoon shows where some of the treatments for MG
act.
Dr. Kaminski will discuss studies being done now that attempt to improve on existing
treatments. Some of the studies are only being studied in animals and cells, but would be
expected to perhaps help humans sometime in the next 10 years.
Cyclosporine, FK-506,
Myocophenolate
T cells
APC
AChR-Ab Azathioprine
producing B cells
Plasma Exchange
AChR
FcgR
Intravenous Immunoglobulin
C
B cell
MAC
C’
C’
Neuromuscular Junction
Injury