The relationship between classical delayed hypersensitivity, as exemplified by the tuberculin-type skin test, and cellular immunity, here defined as an acquired enhancement of resistance to infection with intracellular microor- ganisms, has long been a subject of investigation. Recently the delayed hyper- sensitivity reaction has been opened to renewed study because in vitro models such as
... [Show full abstract] lymphocyte transformation and macrophage migration inhibitory factor (MIF) 1 production have been developed (1). The work of Mackaness and his group (2) has greatly expanded our understanding of the mechanism of cellular immunity, largely through in vivo studies. The present studies describe a quantitative in vitro model of cellular im- munity in the guinea pig. Oil-induced peritoneal exudate cells from immune and control guinea pigs were cultured overnight with and without three different protein antigens. The cultures were then washed, removing lymphocytes and antigen, and the remaining macrophage monolayers were infected with Listeria monocytogenes. Macrophage bactericidal capacity was evaluated both by sequential visual counting and by quantitative culture of intraceltular bacteria. Both techniques demonstrated that peritoneal exudate macrophages from im- mune animals had a greatly enhanced bacterical capacity when the exudate had been cultured with antigen before infection. Macrophage migration was also inhibited under these conditions.