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Morphologic study on experimental allergic neuritis mediated by T cell line specific for bovine P2 protein in Lewis rats.

Light and electron microscope studies were performed on experimental allergic neuritis (EAN) passively induced in Lewis rats by the intravenous injection of T line cells specific for bovine P2 protein. Histologic changes were almost entirely restricted to the peripheral nervous system, being most severe in the sciatic nerve and lumbosacral nerve roots, whereas the brachial nerve and cervical nerve roots were involved to a lesser extent. The lesions were composed of edema, cellular infiltrates, demyelination, and, subsequently, axonal degeneration. Infiltrated macrophages were observed actively stripping the myelin, and the Schwann cell cytoplasm of affected nerve fibers was pushed to the periphery without distinct evidence of degeneration. The first evidence of pathologic change was severe edema in the sciatic nerve 4 days postinoculation. This edema was demonstrated immunohistochemically by the presence of albumin and fibrinogen in the endoneurial space. Mast cell degranulation was observed in these edematous nerve lesions. The cellular infiltrates which formed perivascular cuffs were composed of not only mononuclear cells but also many granulocytes. In the central nervous system, meningeal cell infiltration was also observed in the spinal cord, and after 7 days postinoculation degeneration of the posterior column was also found. This latter observation is thought to represent degeneration due to axonal damage of lumbosacral posterior roots. These pathologic findings in a T cell-mediated model of EAN were essentially the same as those previously reported in conventionally induced EAN or human Guillain-Barré Syndrome. Thus, T cells specific for bovine P2 protein can induce typical EAN lesions in the Lewis rat. The further investigation of this transfer model of EAN will enable us to clarify the pathogenesis of EAN and Guillain-Barré syndrome.