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The Journal of Immunology, 1974, 113: 387-394.
Copyright © 1974 by The American Association of Immunologists, Inc.

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Experimental Allergic Neuritis: Cells Binding Horseradish Peroxidase Conjugates of Myelin Basic Proteins1,2,

Mauro C. dal Canto3, Anne B. Johnson4, Cedric S. Raine5, Henryk M. Wisniewski and Steven W. Brostoff6

From the Department of Pathology (Neuropathology) and the Rose F. Kennedy Center for Research in Mental Retardation and Human Development, Albert Einstein College of Medicine, Bronx, New York 10461

Abstract

In rabbits with experimental allergic neuritis induced by inoculation with purified bovine peripheral myelin, we have demonstrated mononuclear cells specifically binding a conjugate of horseradish peroxidase and bovine P2 protein. The P2 protein is one of the two basic proteins of peripheral myelin and is unique to the peripheral nervous system. The specifically reactive cells were present in lymph nodes and in infiltrates in dorsal root ganglia, a target organ in this autoimmune disease. Many of the reactive cells in both sites resembled plasma cells and large lymphocytes. No cells bound a conjugate of peroxidase and the encephalitogenic basic protein from bovine central myelin, which appears to be chemically identical and is immunopathologically cross-reactive with P1 protein, the other basic protein of peripheral myelin. These immunopathologic results are consistent with the clinical and histologic findings that peripheral myelin induces only neuritis and not encephalomyelitis despite its content of both P1 and P2 proteins. They suggest that within intact peripheral myelin, the antigenic sites on P1 protein are masked whereas those on P2 protein are free to act as immunogens.

In rabbits immunized with purified P2 protein, lymph nodes also contained cells binding the P2 protein peroxidase conjugate. These animals, however, did not develop definite evidence of experimental allergic neuritis.

Footnotes

1 This work was supported by Grant 721-B-4 from the National Multiple Sclerosis Society and, in part, by Grant NS-02255 from the National Institutes of Health.

2 These results were presented, in part, at the 49th Annual Meeting of the American Association of Neuropathologists, Freeport, Grand Bahama Island, June 1973.

3 Present address: Department of Pathology (Neuropathology), Northwestern University Medical School, Chicago, Illinois.

4 Reprint requests should be addressed to this author.

5 Recipient of National Institutes of Health Research Career Development Award NS-70265.

6 Present address: Department of Neurology, Medical University of South Carolina, Charleston, South Carolina 29401.







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