Interleukin-2 and loss of immunity in experimental Mycobacterium avium infection.

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-2Ralpha) 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.

journal_name

Infect Immun

journal_title

Infection and immunity

authors

Mannering SI,Cheers C

doi

10.1128/iai.70.1.27-35.2002

keywords:

subject

Has Abstract

pub_date

2002-01-01 00:00:00

pages

27-35

issue

1

eissn

0019-9567

issn

1098-5522

journal_volume

70

pub_type

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