Exposure of Normal Monocyte-Derived Dendritic Cells to Human Immunodeficiency Virus Type-1 Particles Leads to the Induction of Apoptosis in Co-Cultured CD4<sup>+</sup> as Well as CD8<sup>+</sup> T Cells
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- Suzuki Satoko
- Section of Serology, Institute of Immunological Science, Hokkaido University
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- Tobiume Minoru
- Section of Serology, Institute of Immunological Science, Hokkaido University
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- Kameoka Masanori
- Section of Serology, Institute of Immunological Science, Hokkaido University
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- Sato Katsuaki
- Department of Cell Processing, The Institute of Medical Science, The University of Tokyo
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- Takahashi Tsuneo A.
- Department of Cell Processing, The Institute of Medical Science, The University of Tokyo
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- Mukai Tetsu
- Department of Virology, Research Institute for Microbial Diseases, Osaka University
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- Ikuta Kazuyoshi
- Section of Serology, Institute of Immunological Science, Hokkaido University
抄録
The depletion of immune T cells by human immunodeficiency virus type-1 (HIV-1) infection is a major mechanism involved in the pathogenesis of AIDS. Here, we examined a possible effector function of blood monocyte-derived dendritic cells (DCs) to induce apoptosis in bystander CD4+ and CD8+ T cells. The DCs were generated by culturing monocytes in the presence of granulocyte-macrophage colony-stimulating factor and interleukin-4. The DCs exposed to HIV-1 particles were co-cultured with healthy donor-derived blood T cells at a ratio of 1:20. Analyses by percent cell mortality, staining with propidium iodide and reactivity with Annexin V revealed the induction of apoptosis in both CD4+ and CD8+ target T cells. Further, this apoptosis occurred without stimulation with mitogens when the cell cycle of target T cells shifted from G0 to G1, probably due to the mitogenic effect of the DCs. Thus, induction of apoptosis in both CD4+ and CD8+ T cells occurred via interaction with DCs adsorbed with HIV-1 particles.
収録刊行物
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- MICROBIOLOGY and IMMUNOLOGY
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MICROBIOLOGY and IMMUNOLOGY 44 (2), 111-121, 2000
Center For Academic Publications Japan
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詳細情報 詳細情報について
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- CRID
- 1570854178104474496
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- NII論文ID
- 130003484825
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- ISSN
- 03855600
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- 本文言語コード
- en
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- データソース種別
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- CiNii Articles