HIV-specific cytotoxic T lymphocyte precursors exist in a CD28-CD8+T cell subset and increase with loss of CD4 T cells
HIV-specific cytotoxic T lymphocyte precursors exist in a CD28-CD8+T cell subset and increase with loss of CD4 T cells
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DOI:
10.1097/00002030-199906180-00005
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发表时间:
1999-06-18
期刊:
影响因子:
3.8
通讯作者:
Rodgers, JR
中科院分区:
文献类型:
--
作者:
Lewis, DE;Yang, LX;Rodgers, JR
Objectives: To determine whether the CD28-CD8+ T cells that develop during HIV infection contain HIV-specific cytotoxic precursor cells.Design: CD8 subpopulations from six asymptomatic HIV-positive adults, with varying degrees of CD4 T cell loss, were sorted by flaw cytometry and HIV-specific precursor cytotoxic T lymphocyte frequencies were measured. Three populations of CD8 T cells were tested: CD28+CD57- T cells, CD28-CD57+ T cells (thought to be memory cells) and CD28-CD57- T cells (function unknown).Methods: Sorted CD8 subsets were stimulated with antigen presenting cells expressing HIV-1 Gag/Pol molecules. Cytotoxic T cell assays on Gag/Pol expressing Cr-51-labeled Epstein-Barr virus transformed autologous B cells lines or control targets were performed after 2 weeks. Specific lysis and precursor frequencies were calculated.Results: Both CD28 positive and CD28-CD57+ populations contained appreciable numbers of precursors (9-1720 per 10(6) CD8+ T cells). However, the CD28-CD57-population had fewer precursors in five out of six people studied. More CD28 positive HIV-specific cytotoxic T lymphocyte precursors were found in patients with CD4:CD8 ratios > 1, whereas more CD28-CD57+ precursors were found in patients whose CD 1 : CD8 ratios were < 1 (r(2), 0.68).Conclusions: Memory HIV-specific precursor cytotoxic T lymphocytes are found in both CD28 positive and CD28-CD8+ cells, however, a CD28-CD57-subpopulation had fewer. Because CD28-CD57+ cells are antigen-driven with limited diversity, the loss of CD28 on CD8 T cells during disease progression may reduce the response to new HIV mutations; this requires further testing. (C) 1999 Lippincott Williams & Wilkins.