Abstract
In order to approach the mechanism of chronic or relapsing course in human chronic inflammatory demyelinating polyradiculoneuropathy, we established a chronic model of experimental allergic neuritis (EAN) in juvenile guinea pigs, and investigated the underlying cellular immune phenomenon in comparison with acute EAN in adult animals of the same strain. Two-week-old Hartley guinea pigs, sensitized with bovine peripheral nerve homogenate, developed chronic or relapsing EAN, whereas all adult animals developed acute monophasic EAN. Morphological examination of both the chronic and acute forms revealed scattered demyelination and mononuclear cell infiltrates which were essentially restricted to the peripheral nervous system, and indistinguishable from each other. Both the in vitro lymphocyte mitogenic response and in vivo skin testing revealed a significantly lower response to neuritogenic antigens (P2 protein and peripheral nerve myelin) in juvenile chronic EAN than in adult acute EAN throughout their respective courses. In addition, we showed, by means of assessing peripheral blood lymphocyte number and its subpopulations, that normal 2-week-old Hartley guinea pigs have not fully developed immunologically. These observations suggested that there was some immunological incompetence especially in cellular immunity in 2-week-old juvenile guinea pigs and that this might be one possible factor leading to chronic EAN.
Published Version
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