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Infection and Immunity, January 2002, p. 27-35, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.27-35.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Interleukin-2 and Loss of Immunity in Experimental Mycobacterium avium Infection

Department of Microbiology and Immunology, University of Melbourne, Victoria 3010, Australia

Received 14 May 2001/ Returned for modification 16 July 2001/ Accepted 21 September 2001

Experimental infection of mice with a virulent strain of Mycobacterium avium leads to a slowly progressive disease, which we have previously shown culminates in loss of gamma interferon (IFN-) production by T lymphocytes and death of the animals approximately 40 weeks after infection. Here we investigated the changes in T-cell activation, the production of interleukin-2 (IL-2), and the response to IL-2 throughout M. avium infection as a possible explanation for this loss. We found that there is a steady increase in the percentage of T cells expressing activation markers right to the end of infection. However, in vivo T-cell proliferation, measured as a percentage of CD4⁺ and CD8⁺ cells incorporating 5-bromo-2'-deoxyuridine, initially increased but then remained constant. In the final stages of infection there was a decline in proliferation of activated (CD62L^-) T cells. Since IL-2 is a major driver of T-cell proliferation, we asked whether this was due to loss of IL-2 responsiveness or production. However, CD25 (IL-2R) continued to be highly expressed in the terminal stages of infection, and although IL-2 production declined, addition of recombinant IL-2 to cultures could not rescue the final loss of IFN- production.

Editor: S. H. E. Kaufmann

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