Depression of phagocytic activity and immune response by methyl palmitate

Abstract
Intravenous administration of methyl palmitate produced a marked depression of the phagocytic activity of the RES. Histological evidence indicates that the RE-depressant effect exerted by methyl palmitate is not due to destruction of RE cellular elements but rather to an interference with the phagocytic activity of Kupffer cells. The functional activity of parenchymal cells was unaltered in RE hypofunctional mice. A depressed functional state of the RES, existing at the time of antigenic challenge with sheep erythrocytes, was associated with a profound inhibition of antibody formation during the primary and secondary immune response. This reduced antibody formation was not associated with alterations in the total circulating leukocyte level nor in the percentage of lymphocytes in peripheral blood. The employment of methyl palmitate to produce phagocytic and immunological paralysis is proposed.