期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 99, 期 24, 页码 15572-15577出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.242358099
关键词
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资金
- NCRR NIH HHS [RR06555, R01 RR006555] Funding Source: Medline
- NIAID NIH HHS [R37 AI028433, AI40387, AI28433, R01 AI028433] Funding Source: Medline
Deuterated glucose labeling was used to measure the in vivo turnover of T lymphocytes. A realistic T cell kinetic model, with populations of resting and activated T cells, was fitted to D-glucose labeling data from healthy and HIV-1-infected individuals before and after antiretroviral treatment. Our analysis highlights why HIV-1 infection, which increases the fraction of both CD4(+) and CD8(+) T lymphocytes that are proliferating (Ki67(+)), leads to CD4 but not CD8 depletion. We find that HIV-1 infection tends to increase the rates of death and proliferation of activated CD4(+) T cells, and to increase the rate at which resting CD4 T cells become activated, but does not increase the fraction of activated CD4(+) T cells, consistent with their preferential loss in HIV-1-infected individuals. In contrast, HIV-1 infection does not lead to an increase in proliferation or death rates of activated CD8(+) T cells, but did increase the fraction of activated CD8(+) T cells, consistent with these cells remaining in an activated state longer and undergoing more rounds of proliferation than CD4(+) T cells. Our results also explain why telomeres shorten in CD8(+) cells, but not in CD4(+) cells of HIV-1-infected patients, compared with age-matched controls.
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