What is the role of type-II hypersensitivity reactions in the pathophysiology of myasthenia gravis (MG)?

Updated: Aug 27, 2018
  • Author: Abbas A Jowkar, MBBS; Chief Editor: Nicholas Lorenzo, MD, CPE, MHCM, FAAPL  more...
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It is thought that both the initiation and maintenance of MG occurs in a process that involves type-II hypersensitivity reactions. The production of autoantibodies implies that it is a B-cell-mediated autoimmune disorder. The intiation of the process is dependent on T-cell help. Accordingly, CD4 T cells are the main driving force in the immunopathogenesis of MG. Macrophages and dendritic cells are activated and these act as antigen-presenting cells. AChRs phagocytized by macrophages become degraded into peptide subcomponents. These are then linked to MHC-II, the molecule required for reactivity to “self-antigens.” The AChR antigenic fragment and MHC complex are transported to the surface of macrophages and dendritic cells. Specific, helper T cells, with the cooperation of CD3 complex and CD4 molecular T-cell receptor site, recognize this antigen complex. Specific receptor sites on the T-cell surface recognize cytokines secreted by the macrophage and dendritic cells. The activated helper T cells secrete interferon (IFN)-γ and interleukin (IL)-17 that stimulate B lymphocytes. The activated B lymphocytes grow and undergo clonal expansion into antibody-synthesizing plasma cells. These plasma cells secrete IgG anti-AChR antibodies that bind to the nictonic ACh-R.

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