The influence of immunologically committed lymphoid cells on macrophage activity in vivo was studied. Mice infected with Listeria monocytogenes developed immunologically committed lymphoid cells in their spleens, which could confer protection and delayed-type hypersensitivity to normal recipients. These cells were most numerous on the 6th or 7th day of infection and persisted for at least 20 days. The protection conferred by these cells was dependent on their viability and their ability to multiply in the recipient's tissues. The antibacterial resistance was not due to antibacterial antibody but was mediated through the activation of the recipient's macrophages. This activation appeared to depend on a specific interaction between the immune lymphoid cells and the infecting organism. Immune lymphoid cells from BCG-immunized donors, which were highly resistant to Listeria, failed to protect normal recipients unless the recipients were also injected with an eliciting dose of BCG. The peritoneal macrophages of animals so treated developed the morphology and microbicidal features of activated macrophages. It is inferred that acquired resistance depends on the activation of host macrophages through a product resulting from specific interaction between sensitized lymphoid cells and the organism or its antigenic products. The study also suggests that the activation of macrophages could be dependent on antigenic stimulation of macrophages sensitized by a cytophilic antibody. The findings indicate that immune lymphoid cells can confer protection through indirect means, such as activating macrophages, rather than directly killing the pathogen. The study highlights the importance of immunologically committed lymphoid cells in the host's defense against intracellular pathogens like Listeria monocytogenes.The influence of immunologically committed lymphoid cells on macrophage activity in vivo was studied. Mice infected with Listeria monocytogenes developed immunologically committed lymphoid cells in their spleens, which could confer protection and delayed-type hypersensitivity to normal recipients. These cells were most numerous on the 6th or 7th day of infection and persisted for at least 20 days. The protection conferred by these cells was dependent on their viability and their ability to multiply in the recipient's tissues. The antibacterial resistance was not due to antibacterial antibody but was mediated through the activation of the recipient's macrophages. This activation appeared to depend on a specific interaction between the immune lymphoid cells and the infecting organism. Immune lymphoid cells from BCG-immunized donors, which were highly resistant to Listeria, failed to protect normal recipients unless the recipients were also injected with an eliciting dose of BCG. The peritoneal macrophages of animals so treated developed the morphology and microbicidal features of activated macrophages. It is inferred that acquired resistance depends on the activation of host macrophages through a product resulting from specific interaction between sensitized lymphoid cells and the organism or its antigenic products. The study also suggests that the activation of macrophages could be dependent on antigenic stimulation of macrophages sensitized by a cytophilic antibody. The findings indicate that immune lymphoid cells can confer protection through indirect means, such as activating macrophages, rather than directly killing the pathogen. The study highlights the importance of immunologically committed lymphoid cells in the host's defense against intracellular pathogens like Listeria monocytogenes.