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Autocrine Production of β-Chemokines Protects CMV-Specific CD4+ T Cells from HIV Infection.
- Source :
- PLoS Pathogens; Oct2009, Vol. 5 Issue 10, p1-13, 13p, 1 Chart, 6 Graphs
- Publication Year :
- 2009
-
Abstract
- Induction of a functional subset of HIV-specific CD4<superscript>+</superscript> T cells that is resistant to HIV infection could enhance immune protection and decrease the rate of HIV disease progression. CMV-specific CD4<superscript>+</superscript> T cells, which are less frequently infected than HIV-specific CD4<superscript>+</superscript> T cells, are a model for such an effect. To determine the mechanism of this protection, we compared the functional response of HIV gag-specific and CMV pp65-specific CD4<superscript>+</superscript> T cells in individuals co-infected with CMV and HIV. We found that CMV-specific CD4<superscript>+</superscript> T cells rapidly up-regulated production of MIP-1α and MIP-1β mRNA, resulting in a rapid increase in production of MIP-1α and MIP-1β after cognate antigen stimulation. Production of β-chemokines was associated with maturational phenotype and was rarely seen in HIV-specific CD4<superscript>+</superscript> T cells. To test whether production of b-chemokines by CD4<superscript>+</superscript> T cells lowers their susceptibility to HIV infection, we measured cellassociated Gag DNA to assess the in vivo infection history of CMV-specific CD4<superscript>+</superscript> T cells. We found that CMV-specific CD4<superscript>+</superscript> T cells which produced MIP-1β contained 10 times less Gag DNA than did those which failed to produce MIP-1β. These data suggest that CD4<superscript>+</superscript> T cells which produce MIP-1α and MIP-1β bind these chemokines in an autocrine fashion which decreases the risk of in vivo HIV infection. [ABSTRACT FROM AUTHOR]
- Subjects :
- AUTOCRINE mechanisms
CELLULAR control mechanisms
HIV infections
T cells
CHEMOKINES
Subjects
Details
- Language :
- English
- ISSN :
- 15537366
- Volume :
- 5
- Issue :
- 10
- Database :
- Complementary Index
- Journal :
- PLoS Pathogens
- Publication Type :
- Academic Journal
- Accession number :
- 45438857
- Full Text :
- https://doi.org/10.1371/journal.ppat.1000646