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Anergy, IFN- Production, and Apoptosis in Terminal Infection of Mice with Mycobacterium avium¹

Department of Microbiology and Immunology, University of Melbourne, Parkville, Victoria, Australia

We have followed the course of experimental infection of mice with Mycobacterium avium over an extended period, assessing bacterial numbers and T cell responsiveness. When mice were infected intranasally, bacteria spread to the spleen and liver, but remained in highest numbers in the lungs. Both CD4⁺ and CD8⁺ T cells, assayed at any time from 6–28 wk after infection, produced IFN-. After initial rapid growth, bacterial numbers slowly increased from 10⁷ at 6 wk to more than 5 x 10⁸ at 28 wk, indicating that the resistance mechanisms so generated were not adequate to contain the infection. During infection, apoptosis of both CD4⁺ and CD8⁺ T cells, measured immediately ex vivo by staining with Annexin V, increased steadily. With some individual exceptions, there was a close correlation between apoptosis of CD4⁺ cells and level of IFN- production by cultured spleen cells. By 34 wk postinfection, there was an abrupt cessation of IFN- production. No IL-4 was detected, ruling out a switch to Th2 profile. Subsequently, bacterial numbers increased still further to >5 x 10⁹ per lung, and the mice lost body weight and would have died if not killed for experimental or humane reasons. The possibility that T cells exposed over this prolonged period to extremely high doses of Ag may become tolerant by a process of terminal differentiation is discussed.

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