This study investigates the role of immunologically committed lymphoid cells in mediating macrophage activity and providing protection against *Listeria monocytogenes* infection in mice. The research demonstrates that specific immunity and delayed-type hypersensitivity are concurrently conferred when living lymphoid cells from the spleens of *Listeria*-infected mice are injected into normal recipients. Key findings include: 1. **Development of Immunologically Active Lymphoid Cells**: Immune lymphoid cells are most numerous in the spleen on the 6th or 7th day of infection and persist for at least 20 days. The efficiency of protection increases from the 4th to the 6th or 7th day. 2. **Protective Immunity and Delayed Hypersensitivity**: The protective effect of immune lymphoid cells is dose-dependent, with larger numbers of cells providing greater protection. The cells must be viable to confer protection, and their activity is not due to antibacterial antibodies but rather to the activation of recipient macrophages. 3. **Specificity of Immune Response**: The protection conferred by immune lymphoid cells is specific to *Listeria*, as lymphoid cells from BCG-immunized donors did not protect normal recipients against *Listeria* infection unless the recipients were also injected with BCG. 4. **Activation of Macrophages**: The activation of host macrophages is mediated by a humoral factor released by reactive lymphoid cells in the presence of specific antigen. This factor causes changes in macrophage morphology and microbicidal activity, leading to the activation of macrophages. 5. **Recirculation and Proliferation**: The immune lymphoid cells must be alive and able to proliferate in the recipient tissues to provide maximum resistance. The cells may become antigen-sensitive through a process similar to memory cell formation. The study concludes that acquired resistance to *Listeria* is mediated by the activation of host macrophages through a product resulting from specific interaction between sensitized lymphoid cells and the infecting organism.This study investigates the role of immunologically committed lymphoid cells in mediating macrophage activity and providing protection against *Listeria monocytogenes* infection in mice. The research demonstrates that specific immunity and delayed-type hypersensitivity are concurrently conferred when living lymphoid cells from the spleens of *Listeria*-infected mice are injected into normal recipients. Key findings include: 1. **Development of Immunologically Active Lymphoid Cells**: Immune lymphoid cells are most numerous in the spleen on the 6th or 7th day of infection and persist for at least 20 days. The efficiency of protection increases from the 4th to the 6th or 7th day. 2. **Protective Immunity and Delayed Hypersensitivity**: The protective effect of immune lymphoid cells is dose-dependent, with larger numbers of cells providing greater protection. The cells must be viable to confer protection, and their activity is not due to antibacterial antibodies but rather to the activation of recipient macrophages. 3. **Specificity of Immune Response**: The protection conferred by immune lymphoid cells is specific to *Listeria*, as lymphoid cells from BCG-immunized donors did not protect normal recipients against *Listeria* infection unless the recipients were also injected with BCG. 4. **Activation of Macrophages**: The activation of host macrophages is mediated by a humoral factor released by reactive lymphoid cells in the presence of specific antigen. This factor causes changes in macrophage morphology and microbicidal activity, leading to the activation of macrophages. 5. **Recirculation and Proliferation**: The immune lymphoid cells must be alive and able to proliferate in the recipient tissues to provide maximum resistance. The cells may become antigen-sensitive through a process similar to memory cell formation. The study concludes that acquired resistance to *Listeria* is mediated by the activation of host macrophages through a product resulting from specific interaction between sensitized lymphoid cells and the infecting organism.