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57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

German Society for Neuropathology and Neuroanatomy

12. - 15.09.2012, Erlangen

57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

An autoimmune peripheral nerve model using a human non-myelin antigen

Meeting Abstract

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  • presenting/speaker Colin Crawford - Retired, London, United Kingdom
  • Peter Hardwicke - Southern Illinois University, Biochemistry and Molecular Biology, Carbondale, United States

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Erlangen, 12.-15.09.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12dgnnPP5.3

doi: 10.3205/12dgnn103, urn:nbn:de:0183-12dgnn1035

Published: September 11, 2012

© 2012 Crawford et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Patients with non-lepromatous, paucobacillary leprosy can develop acute sensory loss with simultaneous involvement in all four limbs. In the dermis of the swollen hand in the acute phase, there is a mononuclear cell infiltrate but Mycobacterium leprae are absent. These findings suggest that sensory loss in leprosy could be an autoimune response to an antigen in sensory peripheral nerve rather than a direct invasion of the nerve by M.leprae. In order to test this hypothesis, rabbits were injected with an homogenate of human sural nerve or dorsal roots plus Freunds's Complete Adjuvant. Skin lesions similar to the human disease were produced. Some of the injected rabbits have subsequently developed a state of granulomatous skin testing with dilute concentrations of sensory nerve in saline have produce an epithelioid cell granuloma. These cells contain extensive rough endoplasmic reticulum filled with an electron dense product similar to the cells in berrylium hpersensitivity and sensitivity to zirconium. Some of the cells have invaded the dermal nerves and there are axonal degenerative changes. Thin myelin sheaths are present and also evidence of remyelination. The most active fraction in producing these changes is a deoxycholate extracted membrane fraction from non-myelin peripheral nerve. This is active at concentration levels of 1 mg/ml. Plasma like cells with subplasmalemmal linear densities (SPLDs) are present and could be plasmacytoid dendritic cells.

Strain 13 but not Strain 2 guinea pigs injected in the footpad with a non-myelin homogenate plus adjuvant have developed systemic skin lesions with inflammatory cells invading dermal nerves and axonal degeneration and demyelination. In both experiments there is no evidence of phagocytosis.

The presence of plaques, axonal degenerative changes, absence of phagocytosing macrophages and 'plasma like' cells with SPLDs are features similar to those occurring in multiple sclerosis, but not in experimental allergic encephalomyelitis and indicate that a non-myelin antigen may be implicated in the pathogenesis of multiple sclerosis.