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Tumor necrosis factor-α (TNF-α) plays a key role in the pathogenesis of experimental autoimmune neuritis (EAN) as well as Guillain-Barrè syndrome. The proposed pathogenesis of TNF-α associated neuropathies involves immune-mediated attack to blood-nerve barrier, aggravated production of pro-inflammatory cytokines, and the induction of Schwann cells apoptosis. TNF-α may play a regulatory role by increasing production of interleukin-1 in macrophages, attenuating T cell receptor signaling and regulating apoptosis of potentially autoreactive T cells in EAN. The data suggest that antagonizing TNF-α functions or suppressing TNF-α production may be useful in the acute phase of EAN treatment, but further studies are required.
The proposed pathogenesis of TNF-α associated neuropathies involves immune-mediated attack to blood-nerve (EAN) as well as Guillain-Barré syndrome. barrier, aggravated production of pro-inflammatory cytokines, and the induction of Schwann cell apoptosis. TNF-α may play a regulatory role by increasing production of interleukin-1 in macrophages, attenuating T cell receptor signaling and regulating apoptosis of potentially autoreactive T cells in EAN. The data suggest that antagonizing TNF-α functions or suppressing TNF-α production may be useful in the acute phase of EAN treatment, but further studies are required.