THE IMMUNOLOGICAL BASIS OF ACQUIRED CELLULAR RESISTANCE

G. B. Mackaness

The Journal of Experimental Medicine · 1964 · 798 citations · 13 references

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TL;DR

Acquired resistance in mice to Listeria, Brucella, or Mycobacterium is not organism‑specific but depends on host immunological reactivity and the presence of specific microbial antigens, a relationship that informs understanding of latent infection and immunity. Resistance may arise from altered macrophage function, where antigen–specific antibodies adsorbed to macrophage surfaces interact, possibly involving the same antibody that mediates delayed‑type hypersensitivity. When host immunological reactivity and specific antigens coexist in tissues, mice become non‑specifically resistant.

Abstract

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.

References

13