Abstract
Injection of 6×109 sheep's red blood cells into mice led to suppression of hypersensitivity of delayed type (HDT) in situ and caused activation of spleen cells suppressing sensitization of the recipients. Preliminary thymectomy on the donors and treatment of the cell suspensions with anti-T-globulin abolished the suppressor effect. Preliminary injection of small doses of cyclophosphamide potentiated both the response of antibody formation and the formation of HDT. With an increase in the dose of cyclophosphamide antibody formation was depressed and the HDT response further intensified. The results suggest that suppression of HDT is due to short-living, intensively proliferating cells of thymus origin and also, perhaps, B-cells.
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