Journal
JOURNAL OF IMMUNOLOGY
Volume 188, Issue 3, Pages 1156-1167Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1102610
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Funding
- Canadian Institutes for Health Research
- Fonds de la Recherche en Sante du Quebec Reseau Sida et Maladies Infectieuses
- National Institutes of Health [IDPIDA028871-01]
- Office of Tourism, Trade, and Economic Development of Florida
- MRC [G0501963] Funding Source: UKRI
- Medical Research Council [G0501963] Funding Source: researchfish
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Persistent exposure to cognate Ag leads to the functional impairment and exhaustion of HIV-specific CD8 T cells. Ag withdrawal, attributable either to antiretroviral treatment or the emergence of epitope escape mutations, causes HIV-specific CD8 T cell responses to wane over time. However, this process does not continue to extinction, and residual CD8 T cells likely play an important role in the control of HIV replication. In this study, we conducted a longitudinal analysis of clonality, phenotype, and function to define the characteristics of HIV-specific CD8 T cell populations that persist under conditions of limited antigenic stimulation. Ag decay was associated with dynamic changes in the TCR repertoire, increased expression of CD45RA and CD127, decreased expression of programmed death-1, and the emergence of polyfunctional HIV-specific CD8 T cells. High-definition analysis of individual clonotypes revealed that the Ag loss-induced gain of function within HIV-specific CD8 T cell populations could be attributed to two nonexclusive mechanisms: 1) functional improvement of persisting clonotypes; and 2) recruitment of particular clonotypes endowed with superior functional capabilities. The Journal of Immunology, 2012, 188: 1156-1167.
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