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Interferon‐γ potentiates antibody‐mediated demyelination in vivo
Author(s) -
Vass Karl,
Heininger Kurt,
Schäfer Bärbel,
Linington Christopher,
Lassmann Hans
Publication year - 1992
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410320212
Subject(s) - myelin oligodendrocyte glycoprotein , multiple sclerosis , myelin , immunology , oligodendrocyte , medicine , encephalomyelitis , antibody , monoclonal antibody , interferon , experimental autoimmune encephalomyelitis , central nervous system
The pathogenetic events leading to demyelination in experimental allergic encephalomyelitis and in human multiple sclerosis are still unclear. The involvement of antimyelin antibodies and activated macrophages as effector cells has been postulated. We investigated the synergistic action of the monoclonal antibody 8‐18C5 against myelin/oligodendrocyte glycoprotein and recombinant interferon‐γ on demyelination after simultaneous injection into the subarachnoid space of Sprague‐Dawley rats. After combined injection of anti–myelin/oligodendrocyte glycoprotein antibody and interferon‐γ, electrophysiological and morphological evidence for demyelination was found. Cervical somatosensory evoked potentials and cervical short‐latency somatosensory evoked potentials were significantly delayed, and the demyelinated area in the spinal cord was significantly enlarged when compared to control rats injected with either compound alone. Injection of either an irrelevant antibody and interferon‐γ or of peritoneal macrophages without anti‐myelin/oligodendrocyte glycoprotein antibody and interferon‐γ did not induce demyelination. Our data suggest that the deleterious effect of interferon‐γ on multiple sclerosis may be not only due to its effect on antigen presentation but also due to potentiation of demyelination.