SERUM HEMATOPOIETIC INHIBITORS AND TUMOR NECROSIS FACTOR

Abstract

This chapter discusses serum hematopoietic inhibitors and the tumor necrosis factor (TNF). The presence of colony stimulating activity (CSA) is demonstrable in the serum and urine of norm al humans and mice and is elevated following viral or bacterial infections. In addition, the elevation in serum level of CSA has also been reported following injections of bacterial endotoxin or antigen in experimental mice. It has been proposed that endotoxin may be of central importance in regulation of granulopoiesis and monocyte production because of its capacity to stimulate CSA-release and synthesis by the widely disseminated phagocytic mononuclear cell population. The existence of negative feedback control of granulopoiesis has been postulated as a requirement to counterbalance the positive feedback mediated by CSA, and numerous reports attest to the existence of humeral granulopoietic inhibitors. The capacity of serum to stimulate granulocytic colony formation in vitro is determined by CSA content and by at least two other serum factors. It has become apparent that the two biological activities are separate entities and that the inhibition of colony growth by purified TNF was specific and was not due to the glycoprotein nature of TNF.