Fig. 1. The possible pathogenesis hypothesis of achalasia: susceptible individuals with genetic background, are affected by viruses or other environmental factors, which subsequently triggers an autoimmune response that involved many mediators such as cytokines, chemokines, autoantibodies, complements, and extracellular proteolytic enzymes. Correspondingly, mast cells, eosinophils, and T lymphocytes cross-talk with each other to mediate inflammation, causing the degeneration or loss of myenteric nerve plexus inhibitory neurons. VZV, varicella-zoster virus; MV, measles virus; HSV, herpes simplex virus; CMV, cytomegalovirus; T cell, thymus-dependent lymphocyte; B cell, bursa dependent lymphocyte; APC, antigen-presenting cell.
© J Neurogastroenterol Motil
