Fever Accompanying Delayed Hypersensitivity

Although fever has long been recognized as a cardinal manifestation of hypersensitivity, surprisingly little is known about the mechanisms by which antigens bring about changes in body temperature in hosts with delayed hypersensitivity (1, 2). There is a growing body of evidence tha t in this immunologic state antigen reacts with specifically sensitized lymphocytes to produce soluble mediators, collectively known as lymphokines, tha t induce a var iety of biologic effects, both in vivo and in vitro, such as cytotoxicity, inhibition of macrophage migration, t ransformation of normal lymphocytes, chemotaxis, and others (3, 4). I t is not known whether such substances are involved directly or indirectly in fevers induced by injection of antigen into hosts with delayed hypersensitivity. The following studies were designed to determine if lymphocytes play an essential role in the release of endogenous pyrogen (EP) 1 and hence in the pathogenesis of fever in rabbits with delayed hypersensitivity induced by two heterologous proteins, bovine gamma globulin (BGG) or bovine serum albumin (BSA) conjugated to dinitrophenol (DNP) or by unconjugated human serum albumin (HSA).