From work reported so far it is possible to draw certain conclusions namely, that
Tuftsin,
Thr-Lys-Pro-Arg, is a biologically functional entity. The presence of congenital familial deficiency reinforces this conclusion. The fact that these patients suffer from repeated
infections points at an in vivo system that parallels the in vitro studies showing
tuftsin stimulation of the phagocytic activity of the tissue macrophage and blood granulocyte. Such stimulation occurs at hormonal concentrations; (half maximal at 100 M). Furthermore,
tuftsin enchances pinocytosis, as it does phagocytosis, only in phagocytic cells. It stimulates the motility of these cells as well as their longevity.
Tuftsin stimulates the hexosemonophosphate shunt and, presumably through the formation of
active oxygen-derived compounds, augments the bactericidal as well as the tumoricidal activity of the macrophage. There are highly specific receptors on the cell membrane of phagocytic cells. The structure of
tuftsin cannot be altered without producing inactive and/or inhibitory analogs, an exception being the interchange of
lysine and
arginine. The release of
tuftsin from carrier leukokinin requires two
enzymes, one of which is on the outer membrane of the phagocyte and the other in the spleen. The absence of the latter explains the deficiency observed after the abrogation of splenic function for whatever cause.