Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 39, Issue 5, Pages 1280-1287Publisher
WILEY
DOI: 10.1002/eji.200839002
Keywords
HIV antigens; HIV type 1; IL-10; Treg
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Funding
- K.T.
- Clinical Research Program
- Global Health Program
- Norwegian Functional Genomics Program, Research Council of Norway
- UCSF AIDS Biology Program of the AIDS Research Institute (ARI)
- NIH [AI068498]
- Irvington Institute Fellowship Program of the Cancer Research Institute
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Recent studies have indicated that Treg contribute to the HIV type 1 (HIV-1)-related immune pathogenesis. However, it is not clear whether T cells with suppressive properties reside within the HIV-1-specific T-cell population. Here, PBMC from HIV-1-infected individuals were stimulated with a 15-mer Gag peptide pool, and HIV-1-specific T cells were enriched by virtue of their secretion of IL-10 or IFN-gamma using immunomagnetic cell-sorting. Neither the IL-10-secreting cells nor the IFN-gamma-secreting cells expressed the Treg marker FOXP3, yet the IL-10-secreting cells potently suppressed anti-CD3/CD28-induced CD4(+) as well as CD8(+) T-cell proliferative responses. As shown by intracellular cytokine staining, IL-10- and IFN-gamma-producing T cells represent distinct subsets of the HIV-1-specific T cells. Our data collectively suggest that functionally defined HIV-1-specific T-cell subsets harbor potent immunoregulatory properties that may contribute to HIV-1-associated T-cell dysfunction.
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