Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 207, Issue 13, Pages 2869-2881Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20100090
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Funding
- European Commission [ICA_CT-1999-10007, ICA_CT-2002-10048, E.C. DGVIII - AIDCO - SANTE/2006/129-931]
- Netherlands Organisation for Scientific Research WOTRO [01.53.2004.025]
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HIV-1 infection results in the progressive loss of CD4 T cells. In this study, we address how different pathogen-specific CD4 T cells are affected by HIV infection and the cellular parameters involved. We found striking differences in the depletion rates between CD4 T cells to two common opportunistic pathogens, cytomegalovirus (CMV) and Mycobacterium tuberculosis (MTB). CMV-specific CD4 T cells persisted after HIV infection, whereas MTB-specific CD4 T cells were depleted rapidly. CMV-specific CD4 T cells expressed a mature phenotype and produced very little IL-2, but large amounts of MIP-1 beta. In contrast, MTB-specific CD4 T cells were less mature, and most produced IL-2 but not MIP-1 beta. Staphylococcal enterotoxin B-stimulated IL-2-producing cells were more susceptible to HIV infection in vitro than MIP-1 beta-producing cells. Moreover, IL-2 production was associated with expression of CD25, and neutralization of IL-2 completely abrogated productive HIV infection in vitro. HIV DNA was found to be most abundant in IL-2-producing cells, and least abundant in MIP-1 beta-producing MTB-specific CD4 T cells from HIV-infected subjects with active tuberculosis. These data support the hypothesis that differences in function affect the susceptibility of pathogen-specific CD4 T cells to HIV infection and depletion in vivo, providing a potential mechanism to explain the rapid loss of MTB-specific CD4 T cells after HIV infection.
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