{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,28]],"date-time":"2025-09-28T10:54:21Z","timestamp":1759056861955},"reference-count":38,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2003,7,17]],"date-time":"2003-07-17T00:00:00Z","timestamp":1058400000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2003,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Myelin\u2010sensitized T\u2010 and B\u2010cells (lymph node cells) induced experimental autoimmune neuritis (EAN) in Lewis rats after passive transfer to naive recipients. After 6 days, all recipient rats developed tail paresis that progressed to limb paresis within 12\u201372 h. Progressive nerve conduction changes consistent with demyelination in the sciatic nerve (conduction block and prolongation of the distal motor latencies) and lumbar nerve roots (initial low F\u2010wave frequencies followed by later prolongation in F\u2010wave latencies) were observed during the disease. For comparison, adoptive transfer experimental autoimmune neuritis (AT\u2010EAN) of differing disease severity was induced by titrating the dose of P2\u2010specific T\u2010cells. In contrast to EAN induced by myelin\u2010sensitized T\u2010 and B\u2010cells, AT\u2010EAN was predominantly associated with rapid nerve conduction changes consistent with axonal dysfunction and degeneration. These findings demonstrate that distinct forms of EAN with different pathophysiological mechanisms are induced by the passive transfer of P2\u2010specific T\u2010cell lines or myelin\u2010specific T\u2010cells and B\u2010cells. The electrophysiological changes in EAN induced by myelin\u2010specific T\u2010 and B\u2010cells are very similar to those seen clinically during acute inflammatory demyelinating polyneuropathy, whereas AT\u2010EAN has less resemblance to axonal forms of Guillain\u2013Barr\u00e9 syndrome. 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