Interleukin-2 and loss of immunity in experimental Mycobacterium avium infection
- Author(s)
- Mannering, SI; Cheers, C;
- Details
- Publication Year 2002-01,Volume 70,Issue #1,Page 27-35
- Journal Title
- INFECTION AND IMMUNITY
- Publication Type
- Journal Article
- Abstract
- 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-gamma) 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 alpha) 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-gamma production.
- Publisher
- AMER SOC MICROBIOLOGY
- Keywords
- HUMAN PULMONARY TUBERCULOSIS; T-CELL SUBSETS; GAMMA-INTERFERON; MICE; APOPTOSIS; MEMORY; ANERGY; NAIVE; RESISTANCE; INHIBITION
- Publisher's Version
- https://doi.org/10.1128/IAI.70.1.27-35.2002
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2002-01-01 12:00:00