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The evidence that TNF\u2010\u03b1, released by autoreactive T cells and macrophages, may contribute to the pathogenesis of immune\u2010mediated demyelinating neuropathies is reviewed. TNF\u2010\u03b1 antagonists (infliximab, etanercept, adalimumab) are indicated for the treatment of advanced inflammatory rheumatic and bowel disease, but these drugs can induce a range of autoimmune diseases that also attack the central and peripheral nervous systems. Case histories and series report on the association between anti\u2013TNF\u2010\u03b1 treatment and various disorders of peripheral nerve such as Guillain\u2013Barr\u00e9 syndrome, Miller Fisher syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy with conduction block, mononeuropathy multiplex, and axonal sensorimotor polyneuropathies. The proposed pathogeneses of TNF\u2010\u03b1\u2013associated neuropathies include both a T\u2010cell and humoral immune attack against peripheral nerve myelin, vasculitis\u2010induced nerve ischemia, and inhibition of signaling support for axons. Most neuropathies improve over a period of months by withdrawal of the TNF\u2010\u03b1 antagonist, with or without additional immune\u2010modulating treatment. Preliminary observations suggest that TNF\u2010\u03b1 antagonists may be useful as an antigen\u2010nonspecific treatment approach to immune\u2010mediated neuropathies in patients with a poor response to, or intolerance of, standard therapies, but further studies are required. 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