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Induction of Killer Cells from Lymphocytes in Pleural Effusion of Advanced Lung Cancer Patients

We analyzed the phenotype and cytotoxic ability of pleural exudative lymphocytes (PLEL) which were obtained from 18 advanced lung cancer patients. Freshly isolated PLEL were mainly CD4(+) T cells and had weak natural killer, autologous tumor killing and lymphokine‐activated killer activities. After...

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Detalles Bibliográficos
Autores principales: Inoue, Yuji, Shijubo, Noriharu, Uede, Toshimitsu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 1990
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5917975/
https://www.ncbi.nlm.nih.gov/pubmed/2172193
http://dx.doi.org/10.1111/j.1349-7006.1990.tb03339.x
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author Inoue, Yuji
Shijubo, Noriharu
Uede, Toshimitsu
author_facet Inoue, Yuji
Shijubo, Noriharu
Uede, Toshimitsu
author_sort Inoue, Yuji
collection PubMed
description We analyzed the phenotype and cytotoxic ability of pleural exudative lymphocytes (PLEL) which were obtained from 18 advanced lung cancer patients. Freshly isolated PLEL were mainly CD4(+) T cells and had weak natural killer, autologous tumor killing and lymphokine‐activated killer activities. After cultivation of PLEL with interleukin‐2, cytotoxicity of PLEL against autologous tumor cells was increased at 2 weeks, but it was remarkably reduced at 4 weeks. When PLEL were stimulated by mitomycin C‐treated autologous tumor cells during culture, autologous tumor killing activity of PLEL was significantly enhanced even after 4 weeks of cultivation. Cold target inhibition analysis and binding inhibition assays using monoclonal antibodies indicated that autologous tumor stimulation could induce major histocompatibility complex class I restricted cytotoxic T lymphocytes specific for autologous tumor cells in some cases.
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spelling pubmed-59179752018-05-11 Induction of Killer Cells from Lymphocytes in Pleural Effusion of Advanced Lung Cancer Patients Inoue, Yuji Shijubo, Noriharu Uede, Toshimitsu Jpn J Cancer Res Regular Papers We analyzed the phenotype and cytotoxic ability of pleural exudative lymphocytes (PLEL) which were obtained from 18 advanced lung cancer patients. Freshly isolated PLEL were mainly CD4(+) T cells and had weak natural killer, autologous tumor killing and lymphokine‐activated killer activities. After cultivation of PLEL with interleukin‐2, cytotoxicity of PLEL against autologous tumor cells was increased at 2 weeks, but it was remarkably reduced at 4 weeks. When PLEL were stimulated by mitomycin C‐treated autologous tumor cells during culture, autologous tumor killing activity of PLEL was significantly enhanced even after 4 weeks of cultivation. Cold target inhibition analysis and binding inhibition assays using monoclonal antibodies indicated that autologous tumor stimulation could induce major histocompatibility complex class I restricted cytotoxic T lymphocytes specific for autologous tumor cells in some cases. Blackwell Publishing Ltd 1990-10 /pmc/articles/PMC5917975/ /pubmed/2172193 http://dx.doi.org/10.1111/j.1349-7006.1990.tb03339.x Text en © 1990 Japanese Cancer Association
spellingShingle Regular Papers
Inoue, Yuji
Shijubo, Noriharu
Uede, Toshimitsu
Induction of Killer Cells from Lymphocytes in Pleural Effusion of Advanced Lung Cancer Patients
title Induction of Killer Cells from Lymphocytes in Pleural Effusion of Advanced Lung Cancer Patients
title_full Induction of Killer Cells from Lymphocytes in Pleural Effusion of Advanced Lung Cancer Patients
title_fullStr Induction of Killer Cells from Lymphocytes in Pleural Effusion of Advanced Lung Cancer Patients
title_full_unstemmed Induction of Killer Cells from Lymphocytes in Pleural Effusion of Advanced Lung Cancer Patients
title_short Induction of Killer Cells from Lymphocytes in Pleural Effusion of Advanced Lung Cancer Patients
title_sort induction of killer cells from lymphocytes in pleural effusion of advanced lung cancer patients
topic Regular Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5917975/
https://www.ncbi.nlm.nih.gov/pubmed/2172193
http://dx.doi.org/10.1111/j.1349-7006.1990.tb03339.x
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