Heightened T-cell proliferation without an elevation of CD4+ T cell spontaneous apoptosis in AIDS patients
T lymphocyte turnover has been studied extensively in HIV infection. The dynamic characteristics of various subsets of T cells in antiretroviral-naive, HIV-1-infected individuals, however, have not been well defined. Here, we performed a cross-sectional study using peripheral blood T cells from 39 a...
| Publié dans: | Clinical immunology (Orlando, Fla.). - 1999. - 129(2008), 3 vom: 17. Dez., Seite 499-508 |
|---|---|
| Auteur principal: | |
| Autres auteurs: | , , , , , , , |
| Format: | Article en ligne |
| Langue: | English |
| Publié: |
2008
|
| Accès à la collection: | Clinical immunology (Orlando, Fla.) |
| Sujets: | Journal Article Research Support, Non-U.S. Gov't Ki-67 Antigen RNA, Viral ADP-ribosyl Cyclase 1 EC 3.2.2.6 |
| Résumé: | T lymphocyte turnover has been studied extensively in HIV infection. The dynamic characteristics of various subsets of T cells in antiretroviral-naive, HIV-1-infected individuals, however, have not been well defined. Here, we performed a cross-sectional study using peripheral blood T cells from 39 antiretroviral-naive, chronically HIV-infected patients, as well as 16 healthy, HIV-negative controls. T-cell subset turnover rates were measured by Ki-67 antigen staining; levels of spontaneous apoptosis and activation in T-cell subsets were also determined by flow cytometry. Surprisingly, with disease progression, the level of T-cell spontaneous apoptosis did not increase significantly, despite a heightened rate of T-cell subset turnover and increased expression of the CD38 activation marker. These data refute the idea that increased T cell turnover is merely a homeostatic process in response to CD4 T cell loss during HIV disease progression, and suggest that future mechanistic studies may be needed for a comprehensive understanding of T-cell dynamics during HIV infection. Such understanding may help to develop new strategies for the immune modulation of clinical disease |
|---|---|
| Description: | Date Completed 04.12.2008 Date Revised 16.11.2017 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1521-7035 |
| DOI: | 10.1016/j.clim.2008.08.004 |