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Allostimulation of patients' lymphocytes generates both T and NK-like cells cytotoxic for autologous melanoma.
Killing of autologous melanoma (auto-Me) was obtained with pooled allostimulated peripheral blood lymphocytes (PBL) in 34/42 cases and found not to be due to a cross-reactivity between melanoma and allogeneic normal antigens. To see whether generation of tumour cytotoxic PBL by allostimulation was d...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
1985
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1977169/ https://www.ncbi.nlm.nih.gov/pubmed/3160380 |
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author | Balsari, A. Fossati, G. Taramelli, D. Tona, G. Delia, D. Giardini, R. Parmiani, G. |
author_facet | Balsari, A. Fossati, G. Taramelli, D. Tona, G. Delia, D. Giardini, R. Parmiani, G. |
author_sort | Balsari, A. |
collection | PubMed |
description | Killing of autologous melanoma (auto-Me) was obtained with pooled allostimulated peripheral blood lymphocytes (PBL) in 34/42 cases and found not to be due to a cross-reactivity between melanoma and allogeneic normal antigens. To see whether generation of tumour cytotoxic PBL by allostimulation was due to release of IL-2, PBL from 34 patients were divided into two aliquots and stimulated either by alloantigens or IL-2. Allostimulated PBL were cytotoxic for auto-Me in 30/34 cases (85%) whereas IL-2 generated tumour cytotoxic cells in 22/34 cases (64%). Lysis of K562, a target for monitoring NK-like activity, was obtained in 95-100% of cases with both stimuli. A similar frequency of OKT3+, OKT4+, OKT8+ and HNK1+ cells was found in PBL activated by allostimulation and IL-2, whereas a higher frequency of OKM1+ cells was evident in IL-2-stimulated PBL. Cold-target competition studies indicated that allostimulation generated at least two different types of effectors, one lytic to auto-Me but not to K562, and the other which lysed both targets. Allostimulated, FACS-separated T3- cells killed both auto-Me and K562 cells whereas T3+ cells lysed only auto-Me. It is concluded that allostimulation generated two subpopulations of auto-Me killer cells, one of the T lineage and the other NK-like, which both can destroy auto-Me targets. |
format | Text |
id | pubmed-1977169 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1985 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-19771692009-09-10 Allostimulation of patients' lymphocytes generates both T and NK-like cells cytotoxic for autologous melanoma. Balsari, A. Fossati, G. Taramelli, D. Tona, G. Delia, D. Giardini, R. Parmiani, G. Br J Cancer Research Article Killing of autologous melanoma (auto-Me) was obtained with pooled allostimulated peripheral blood lymphocytes (PBL) in 34/42 cases and found not to be due to a cross-reactivity between melanoma and allogeneic normal antigens. To see whether generation of tumour cytotoxic PBL by allostimulation was due to release of IL-2, PBL from 34 patients were divided into two aliquots and stimulated either by alloantigens or IL-2. Allostimulated PBL were cytotoxic for auto-Me in 30/34 cases (85%) whereas IL-2 generated tumour cytotoxic cells in 22/34 cases (64%). Lysis of K562, a target for monitoring NK-like activity, was obtained in 95-100% of cases with both stimuli. A similar frequency of OKT3+, OKT4+, OKT8+ and HNK1+ cells was found in PBL activated by allostimulation and IL-2, whereas a higher frequency of OKM1+ cells was evident in IL-2-stimulated PBL. Cold-target competition studies indicated that allostimulation generated at least two different types of effectors, one lytic to auto-Me but not to K562, and the other which lysed both targets. Allostimulated, FACS-separated T3- cells killed both auto-Me and K562 cells whereas T3+ cells lysed only auto-Me. It is concluded that allostimulation generated two subpopulations of auto-Me killer cells, one of the T lineage and the other NK-like, which both can destroy auto-Me targets. Nature Publishing Group 1985-07 /pmc/articles/PMC1977169/ /pubmed/3160380 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Research Article Balsari, A. Fossati, G. Taramelli, D. Tona, G. Delia, D. Giardini, R. Parmiani, G. Allostimulation of patients' lymphocytes generates both T and NK-like cells cytotoxic for autologous melanoma. |
title | Allostimulation of patients' lymphocytes generates both T and NK-like cells cytotoxic for autologous melanoma. |
title_full | Allostimulation of patients' lymphocytes generates both T and NK-like cells cytotoxic for autologous melanoma. |
title_fullStr | Allostimulation of patients' lymphocytes generates both T and NK-like cells cytotoxic for autologous melanoma. |
title_full_unstemmed | Allostimulation of patients' lymphocytes generates both T and NK-like cells cytotoxic for autologous melanoma. |
title_short | Allostimulation of patients' lymphocytes generates both T and NK-like cells cytotoxic for autologous melanoma. |
title_sort | allostimulation of patients' lymphocytes generates both t and nk-like cells cytotoxic for autologous melanoma. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1977169/ https://www.ncbi.nlm.nih.gov/pubmed/3160380 |
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