THE INITIAL LESION IN EXPERIMENTAL ALLERGIC NEURITIS

Author:

Åström Karl E.1,Webster Henry de F.1,Arnason Barry G.1

Affiliation:

1. From the Department of Neurology, the Joseph P. Kennedy, Jr., Laboratories of the Neurology Service, Massachusetts General Hospital; the Department of Neurology-Neuropathology, Harvard Medical School, Boston, Massachusetts 02114; and the Department of Pathology II, Karolinska Institutet, Stockholm, Sweden

Abstract

Experimental allergic neuritis (EAN) was produced in rats by the intradermal injection of an emulsion of peripheral nerve in Freund's adjuvant. Early lesions in perfused sciatic nerves were studied by phase, light, and electron microscopy at intervals up to 15 days following immunization. Circulating lymphocytes attached focally to the inner surface of blood vessels, primarily venules, to initiate parenchymal lesion formation. Attached cells had the hand mirror configuration typical of the motile lymphocyte. They subsequently flattened against the endothelial surface and then traversed the vascular wall by sinking into and passing through the cytoplasm of endothelial cells. The transgressor and transgressed cell membranes were intact and both cells retained their integrity. Lymphocytes began to transform and divide intravascularly; these events accelerated extravascularly. Although the migrating cells became larger and more pleomorphic in the perivascular regions, their essential character was in keeping with an origin from circulating lymphocytes. In many lesions, there was fluid with protein, possibly produced by the transformed extravascular cells. The described cellular events precede tissue damage and are likely instrumental in the myelin destruction which follows

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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