Role of Cytokines and Toll-Like Receptors in the Immunopathogenesis of Guillain-Barré Syndrome

Figure 1

Overview of immunopathogenesis of GBS. A bacterial cross-reactive antigen recognized by macrophages and T cells that help B cells to produce anti-ganglioside antibodies which penetrates blood-nerve barrier and can activate complement. These antibodies bind with specific nerve gangliosides and antigen as well. Activated endoneurial macrophages release cytokines, proteases, and free radicals (nitric oxide, oxygen, and hydrogen peroxide), invade compact myelin and periaxonal space, and sometimes block nerve conduction or cause axonal degeneration. Activated T cell releases proinflammatory cytokines, fixes complement, damages Schwann cell, and ultimately produces dissolution of myelin. The extent of nerve damage depends on several factors. Nerve dysfunction leads to weakness and might cause sensory disturbances. Treatment with IVIg and/or PE helps in recovery from the disease; however despite IVIg/PE treatment, many patients only partially recover and have residual weakness, pain, and fatigue. BNB, blood-nerve barrier; TNF, tumor necrosis factor alpha; IL, interleukin; IFNγ, interferon gamma; APC, antigen presenting cell; TLR, toll-like receptor; Th, helper T cell; IVIg, intravenous immunoglobulin; PE, plasma exchange.