Abstract
Peripheral blood cells, obtained from patients with recurrent hereditary polyserositis (RHP) during attack-free intervals, were found to produce less interferon-γ than cells from healthy controls when stimulated with phytohaemagglutinin. A similar, although less pronounced hyporesponsiveness was observed for interferon-α, produced after stimulation with Sendai virus. Treatment of the patients with colchicine appeared to restore, or partly restore, the interferon-α and interferon-γ responsiveness, although neither interferon could be demonstrated in sera from the patients. However, the RHP patients displayed significantly raised serum levels of β2-microglobulin, a substance whose synthesis is stimulated by interferon. The interferon abnormality in RHP may be a secondary phenomenon, but it cannot be excluded that it has a pathogenetic role in the development of the disease.
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