2024-03-29T13:52:45Z
https://u-ryukyu.repo.nii.ac.jp/oai
oai:u-ryukyu.repo.nii.ac.jp:02012193
2023-08-03T05:31:07Z
1642838163960:1642838338003
1642838403551:1642838407795
T Cell Receptor Vβ Staining Identifies the Malignant Clone in Adult T cell Leukemia and Reveals Killing of Leukemia Cells by Autologous CD8^+ T cells
Rowan, Aileen G.
Witkover, Aviva
Melamed, Anat
Tanaka, Yuetsu
Cook, Lucy B. M.
Fields, Paul
Taylor, Graham P.
Bangham, Charles R. M.
open access
There is growing evidence that CD8^+ cytotoxic T lymphocyte (CTL) responses can contribute to long-term remission of many malignancies. The etiological agent of adult T-cell leukemia/lymphoma (ATL), human T lymphotropic virus type-1 (HTLV-1), contains highly immunogenic CTL epitopes, but ATL patients typically have low frequencies of cytokine-producing HTLV-1-specific CD8^+ cells in the circulation. It remains unclear whether patients with ATL possess CTLs that can kill the malignant HTLV-1 infected clone. Here we used flow cytometric staining of TCRVβ and cell adhesion molecule-1 (CADM1) to identify monoclonal populations of HTLV-1-infected T cells in the peripheral blood of patients with ATL. Thus, we quantified the rate of CD8^+-mediated killing of the putative malignant clone in ex vivo blood samples. We observed that CD8^+ cells from ATL patients were unable to lyse autologous ATL clones when tested directly ex vivo. However, short in vitro culture restored the ability of CD8^+ cells to kill ex vivo ATL clones in some donors. The capacity of CD8^+ cells to lyse HTLV-1 infected cells which expressed the viral sense strand gene products was significantly enhanced after in vitro culture, and donors with an ATL clone that expressed the HTLV-1 Tax gene were most likely to make a detectable lytic CD^8+ response to the ATL cells. We conclude that some patients with ATL possess functional tumour-specific CTLs which could be exploited to contribute to control of the disease.
論文
Public Library of Science
2016-11-28
eng
journal article
VoR
http://hdl.handle.net/20.500.12000/45207
http://hdl.handle.net/20.500.12000/45207
https://u-ryukyu.repo.nii.ac.jp/records/2012193
https://doi.org/10.1371/journal.ppat.1006030
10.1371/journal.ppat.1006030
1553-7366
1553-7374
AA12072310
PLoS Pathogens
12
11
1
20
https://u-ryukyu.repo.nii.ac.jp/record/2012193/files/No12p1.pdf