Summary
Immunity to facultative intracellular bacteria (FIB) rests upon collaboration between antigen-specific T cells and macrophages. Work mostly done in the Listeria infection model in mice has yielded that granulomas are formed and macrophages activated under the influence of specific T lymphocytes which, upon antigen stimulation, secrete lymphokines. Macrophages are activated by MAF (γ interferon) which is secreted both by naturally produced and by cloned Ly 1+T cells, whereas granuloma formation is due to the activity of Ly 12+T cells. Both macrophage activation and granuloma formation contribute to the effective buildup of immunity to FIB, granuloma formation being the more important part. Ly 1+2-T cells are H2-I-A restricted whereas granuloma-inducing Ly 12+T cells are H2-K restricted. The former recognize dead bacterial antigen whereas the latter need antigen produced by viable bacteria. Ly 1+2-T cells with Listeria specificity have been cloned and shown to produce γ interferon, transfer delayed-type hypersensitivity, and transfer systemic macrophage activation.
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Hahn, H., Näher, H. (1985). Interacting T Cell Functions Elicited by Facultative Intracellular Bacteria. In: Jackson, G.G., Thomas, H. (eds) The Pathogenesis of Bacterial Infections. Bayer-Symposium, vol 8. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70351-5_14
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DOI: https://doi.org/10.1007/978-3-642-70351-5_14
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