Abstract
We previously showed the suppression of delayed-type hypersensitivity produced by live BCG-induced, plastic-adhering cells. The present study was undertaken to determine whether prostaglandin was one of the pharmacological mediators involved in this suppression. A high level of prostaglandin E1 was detected in the culture supernatant fluid of the live BCG-induced, adherent cells. Moreover, prostaglandin E1 could suppress the macrophage migration inhibition activity of peritoneal exudate cells from BCG cell wall-sensitized mice.
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