Figure 3: Origin and contribution of antiganglioside antibodies and C. jejuni infection to Guillain-Barré syndrome pathogenesis. A bacterial cross-reactive antigen recognized by macrophages and T cells that help B cells to produce antiganglioside antibodies, which penetrate blood-nerve barrier and activate complement. These antibodies bind with specific nerve gangliosides and C. jejuni antigen as well. Activated endoneurial macrophages release cytokine and free radicals (nitric oxide), invade compact myelin, periaxonal space, and sometimes block nerve conduction or cause axonal degeneration. Activated T cells release proinflammatory cytokines, fix complement, damage Schwann cell, and ultimately produce dissolution of myelin.