The development of acquired cell-mediated immunity to infection with Listeria monocytogenes can be blocked by a 15 hr pulse of the antimitotic drug, vinblastine (Vb). The drug has no effect on the host-parasite relationship after 72 hr of infection when a high level of immunity is being expressed, i.e., when infective foci are populated by activated macrophages. Infective foci in mice treated early during infection with Vb do not acquire migrant macrophages, but they become acellular after 48 hr of infection. The results indicate that Vb destroys the dividing precursors of migrant macrophages. The possibility that Vb prevents the activation of these cells by destroying dividing lymphoid cells engaged in the specific immunological phase of the host response is also considered.

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