Abstract
Cellular hypersensitivity to myelin basic (A
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) protein in relation to clinical attacks of multiple sclerosis was investigated with the technic of macrophage-migration inhibition. Lymphocytes from 48 patients with multiple sclerosis and 24 normal controls were cultured in the presence of human central nervous system basic myelin protein and the culture supernatants assayed for migration-inhibition factor with normal guinea-pig peritoneal macrophages. The controls exhibited a mean (± S.D.) migration of 97 ± 9 per cent, and the patients one of 73.2 ± 16.5 per cent. Twelve patients suspected pected of having multiple sclerosis gave a mean of 73.8 ± 23 per cent. Thirteen with acute "probable" multiple sclerosis gave a mean migration of 61 ± 8.9 per cent, and 12 convalescent patients, one of 78.8 ± 8.3 per cent. Eleven chronic patients studied for six months or longer after their attacks gave a value of 90.9 ± 9 per cent. The results demonstrate a temporal relation between production of migration-inhibition factor (cellular hypersensitivity) to basic myelin protein and clinical attacks of illness in multiple sclerosis. (N Engl J Med 291:14–17, 1974)
MULTIPLE sclerosis and its relation to hypersensitivity to Central-nervous-system antigens has been studied for more than a third of a century. In 1934 Sachs and Steiner
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reported that 42 per cent of patients with multiple sclerosis demonstrated complement-fixing antibodies to brain. However, despite many efforts and a proliferation of methods, no correlation between antibody production and clinical manifestations of disease has been demonstrated. Lymphoblastic transformation, introduced by Hashem and Barr
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as a measure of cellular (delayed) hypersensitivity, has, in a number of reports, given conflicting results.
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The Thor
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and Rocklin
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modifications of the macrophage-migration-inhibition assay has made available an extensively . . .
