The resistance developed by mice during infection with Listeria monocytogenes, Brucella abortus, or Mycobacterium tuberculosis is not specifically directed against the infecting organism. The processes involved in the induction of acquired resistance, however, are highly specific and seem to depend upon two factors: a state of immunological reactivity of the host and the presence of the specific microbial antigens to which the host has become reactive. When these two coexist in the tissues the host is found to be non-specifically resistant. It is suggested that resistance, which was shown to depend upon an altered state of host macrophages, may be due to the interaction of antigen and a specific antibody adsorbed to the surface of host macrophages; and that the antibody involved in the reaction is perhaps identical with the antibody which confers the state of delayed-type hypersensitivity. The results are discussed in relation to the question of latent infection and infection immunity.

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