Cellular Immunity in Vitro

Abstract

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 microorganisms, has long been a subject of investigation. Recently the delayed hypersensitivity reaction has been opened to renewed study because in vitro models such as 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 immunity 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 immune 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. Materials and MethodsAnimals.--Inbred strain 2 guinea pigs of both sexes weighing 200-500 g were used. For the initial studies the guinea pigs were immunized with complete Freund's adjuvant (CFA) containing 5 mg/ml of Mycobacterium tuberculosis H37Ra

The Mediator of Cellular Immunity

“…The events underlying this activation process have not been determined, but they could involve the activity of a lymphokine. In fact, it has been reported recently that a product of antigen-stimulated lymphocytes can influence the microbicidal capacity of macrophages in vitro (25,26).…”

Biological and Biochemical Characterization of Macrophage Activating Factor (MAF) in Murine Lymphocytes: Role of Mannopyranosyl Residue of the MAF Molecule in Macrophage Activation

“…Lymphokineinduced alterations in the behavior of these cells may play an important role in inflammation and cell-mediated immune reactions (19). The enhancement of bactericidal activity against intracellular parasites has been described as one of the important functional properties of macrophages associated with the acquisition of cell-mediated immunity (14,19) and a lymphokine, the macrophage activating factor (MAF), is thought to enhance their bactericidal activity. Little is known, however, about the mechanism(s) by which lymphokines interact with target cells.…”

In Vitro Studies on the Mechanism of Acquired Resistance to Tuberculous Infection

“…Therefore, identity of antigenicity between eliciting antigens and target bacteria may not be required. Reports that cellular resistance to Listeriamonocytogenes can be transferred by BCG-immune lymphoid cells, but its induction requires injection of an eliciting dose of BCG into the recipients [19], and that intracellular growth of L. monocytogenes was inhibited under the influence of BGG-immune lymphoid cells and BGG [9,[26][27][28] seem to support the concept that macrophages are nonspecifically activated to become bactericidal by sensitized lymphocytes stimulated with specific antigens.…”

“…Simon and Sheagren recently showed that macrophages from immune peritoneal exudate cells cultivated with specific antigen before infection had markedly enhanced listericidal activity, but supernatants from stimulated lymphocytes with specific antigen exhibited only substantial migration inhibitory-factor activity but did not enhance the listericidal activity of macrophages [26][27][28]. However, it has to be confirmed whether such correlation between immune lymphoid cells and nonspecific bactericidal activity of macrophages is true or not in the case of M. tuberculosis since the growth rate of tubercle bacilli is much slower than that of Listeria.…”