Differential killing of pre‐B acute lymphoblastic leukaemia cells by activated NK cells and the NK‐92 ci cell line
SUMMARY The use of NK cells in adoptive therapy for malignant disease is an area of great potential. Currently the only NK cell line in clinical trials is NK‐92, an activated NK cell line with a broad range of cytotoxicity against malignant cells. The activity of NK‐92 against pre‐B acute lymphoblas...
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| Veröffentlicht in: | Clinical and experimental immunology 2002-08, Vol.129 (2), p.265-271 |
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| creator | REID, G. S. D. BHARYA, S. KLINGEMANN, H.‐G. SCHULTZ, K. R. |
| description | SUMMARY
The use of NK cells in adoptive therapy for malignant disease is an area of great potential. Currently the only NK cell line in clinical trials is NK‐92, an activated NK cell line with a broad range of cytotoxicity against malignant cells. The activity of NK‐92 against pre‐B acute lymphoblastic leukaemias, however, is highly variable. In this study we compare the cytotoxic mechanisms and signalling pathways utilized by NK‐92 ci and IL‐2 activated NK cells to mediate killing of pre‐B acute lymphoblastic leukaemia cell lines. Deficiencies in TNF family mediated apoptosis, phosphoinositide‐3 kinase dependent and phosphoinositide‐3 kinase independent killing limit the efficiency of NK‐92 ci against pre‐B acute lymphoblastic leukaemia cells. Importantly, treatment of the poorly killed leukaemia cells with TNF‐α augmented both phosphoinositide‐dependent and ‐independent cytolysis. |
| doi_str_mv | 10.1046/j.1365-2249.2002.01919.x |
| format | Article |
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The use of NK cells in adoptive therapy for malignant disease is an area of great potential. Currently the only NK cell line in clinical trials is NK‐92, an activated NK cell line with a broad range of cytotoxicity against malignant cells. The activity of NK‐92 against pre‐B acute lymphoblastic leukaemias, however, is highly variable. In this study we compare the cytotoxic mechanisms and signalling pathways utilized by NK‐92 ci and IL‐2 activated NK cells to mediate killing of pre‐B acute lymphoblastic leukaemia cell lines. Deficiencies in TNF family mediated apoptosis, phosphoinositide‐3 kinase dependent and phosphoinositide‐3 kinase independent killing limit the efficiency of NK‐92 ci against pre‐B acute lymphoblastic leukaemia cells. Importantly, treatment of the poorly killed leukaemia cells with TNF‐α augmented both phosphoinositide‐dependent and ‐independent cytolysis.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1046/j.1365-2249.2002.01919.x</identifier><identifier>PMID: 12165082</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Apoptosis ; Applied cell therapy and gene therapy ; Basic Immunology ; Biological and medical sciences ; Cell Line ; Cytotoxicity, Immunologic ; Humans ; Immunotherapy, Adoptive ; In Vitro Techniques ; Interleukin-2 - pharmacology ; Killer Cells, Natural - immunology ; Medical sciences ; NK‐92 acute lymphoblastic leukaemia cytotoxicity PI‐3 kinase TNF ; Phosphatidylinositol 3-Kinases - metabolism ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - enzymology ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - immunology ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - pathology ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - therapy ; Signal Transduction ; Transfusions. Complications. Transfusion reactions. Cell and gene therapy ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha - metabolism ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>Clinical and experimental immunology, 2002-08, Vol.129 (2), p.265-271</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. Aug 2002</rights><rights>2002 Blackwell Science Ltd 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5589-43b9ce4267d094c534e8359d02a2d03aab447a696cc1f8e77655b6e62636ce903</citedby><cites>FETCH-LOGICAL-c5589-43b9ce4267d094c534e8359d02a2d03aab447a696cc1f8e77655b6e62636ce903</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1906454/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1906454/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13825983$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12165082$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>REID, G. S. D.</creatorcontrib><creatorcontrib>BHARYA, S.</creatorcontrib><creatorcontrib>KLINGEMANN, H.‐G.</creatorcontrib><creatorcontrib>SCHULTZ, K. R.</creatorcontrib><title>Differential killing of pre‐B acute lymphoblastic leukaemia cells by activated NK cells and the NK‐92 ci cell line</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>SUMMARY
The use of NK cells in adoptive therapy for malignant disease is an area of great potential. Currently the only NK cell line in clinical trials is NK‐92, an activated NK cell line with a broad range of cytotoxicity against malignant cells. The activity of NK‐92 against pre‐B acute lymphoblastic leukaemias, however, is highly variable. In this study we compare the cytotoxic mechanisms and signalling pathways utilized by NK‐92 ci and IL‐2 activated NK cells to mediate killing of pre‐B acute lymphoblastic leukaemia cell lines. Deficiencies in TNF family mediated apoptosis, phosphoinositide‐3 kinase dependent and phosphoinositide‐3 kinase independent killing limit the efficiency of NK‐92 ci against pre‐B acute lymphoblastic leukaemia cells. Importantly, treatment of the poorly killed leukaemia cells with TNF‐α augmented both phosphoinositide‐dependent and ‐independent cytolysis.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Apoptosis</subject><subject>Applied cell therapy and gene therapy</subject><subject>Basic Immunology</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cytotoxicity, Immunologic</subject><subject>Humans</subject><subject>Immunotherapy, Adoptive</subject><subject>In Vitro Techniques</subject><subject>Interleukin-2 - pharmacology</subject><subject>Killer Cells, Natural - immunology</subject><subject>Medical sciences</subject><subject>NK‐92 acute lymphoblastic leukaemia cytotoxicity PI‐3 kinase TNF</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - enzymology</subject><subject>Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - immunology</subject><subject>Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - pathology</subject><subject>Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - therapy</subject><subject>Signal Transduction</subject><subject>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNks1u1DAQxyMEokvhFZCFBLcEf8c-gARLgYoKLnC2HGfS9dabLHGydG88As_Ik-DsRi1wgZPtmd_8Z8YzWYYILgjm8vm6IEyKnFKuC4oxLTDRRBfXd7LFjeNutsAY61yniJPsQYzr9JRS0vvZCaFECqzoItu98U0DPbSDtwFd-RB8e4m6Bm17-Pn9x2tk3TgACvvNdtVVwcbBOxRgvLKw8RY5CCGiap-wwe_sADX6-GG22rZGwwqSIQlpipw_OFDKAA-ze40NER7N52n25e3Z5-X7_OLTu_Plq4vcCaF0zlmlHXAqyxpr7gTjoJjQNaaW1phZW3FeWqmlc6RRUJZSiEqCpJJJBxqz0-zlUXc7VhuoXeqzt8Fse7-x_d501ps_Pa1fmctuZ4jGkgueBJ7NAn33dYQ4mI2PUxu2hW6MpiRaYc30P0GiOOeSyAQ--Qtcd2Pfpl9ISaXSFB_qVkfI9V2MPTQ3JRNsphUwazNN2kyTNtMKmMMKmOsU-vj3lm8D55kn4OkM2OhsaHrbOh9vOaao0Iol7sWR--YD7P-7ALM8O59u7Bf85M3z</recordid><startdate>200208</startdate><enddate>200208</enddate><creator>REID, G. S. D.</creator><creator>BHARYA, S.</creator><creator>KLINGEMANN, H.‐G.</creator><creator>SCHULTZ, K. R.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Oxford University Press</general><general>Blackwell Science Inc</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200208</creationdate><title>Differential killing of pre‐B acute lymphoblastic leukaemia cells by activated NK cells and the NK‐92 ci cell line</title><author>REID, G. S. D. ; BHARYA, S. ; KLINGEMANN, H.‐G. ; SCHULTZ, K. R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5589-43b9ce4267d094c534e8359d02a2d03aab447a696cc1f8e77655b6e62636ce903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Apoptosis</topic><topic>Applied cell therapy and gene therapy</topic><topic>Basic Immunology</topic><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Cytotoxicity, Immunologic</topic><topic>Humans</topic><topic>Immunotherapy, Adoptive</topic><topic>In Vitro Techniques</topic><topic>Interleukin-2 - pharmacology</topic><topic>Killer Cells, Natural - immunology</topic><topic>Medical sciences</topic><topic>NK‐92 acute lymphoblastic leukaemia cytotoxicity PI‐3 kinase TNF</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - enzymology</topic><topic>Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - immunology</topic><topic>Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - pathology</topic><topic>Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - therapy</topic><topic>Signal Transduction</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>REID, G. S. D.</creatorcontrib><creatorcontrib>BHARYA, S.</creatorcontrib><creatorcontrib>KLINGEMANN, H.‐G.</creatorcontrib><creatorcontrib>SCHULTZ, K. R.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>REID, G. S. D.</au><au>BHARYA, S.</au><au>KLINGEMANN, H.‐G.</au><au>SCHULTZ, K. R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential killing of pre‐B acute lymphoblastic leukaemia cells by activated NK cells and the NK‐92 ci cell line</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2002-08</date><risdate>2002</risdate><volume>129</volume><issue>2</issue><spage>265</spage><epage>271</epage><pages>265-271</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>SUMMARY
The use of NK cells in adoptive therapy for malignant disease is an area of great potential. Currently the only NK cell line in clinical trials is NK‐92, an activated NK cell line with a broad range of cytotoxicity against malignant cells. The activity of NK‐92 against pre‐B acute lymphoblastic leukaemias, however, is highly variable. In this study we compare the cytotoxic mechanisms and signalling pathways utilized by NK‐92 ci and IL‐2 activated NK cells to mediate killing of pre‐B acute lymphoblastic leukaemia cell lines. Deficiencies in TNF family mediated apoptosis, phosphoinositide‐3 kinase dependent and phosphoinositide‐3 kinase independent killing limit the efficiency of NK‐92 ci against pre‐B acute lymphoblastic leukaemia cells. Importantly, treatment of the poorly killed leukaemia cells with TNF‐α augmented both phosphoinositide‐dependent and ‐independent cytolysis.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>12165082</pmid><doi>10.1046/j.1365-2249.2002.01919.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical and experimental immunology, 2002-08, Vol.129 (2), p.265-271 |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Apoptosis Applied cell therapy and gene therapy Basic Immunology Biological and medical sciences Cell Line Cytotoxicity, Immunologic Humans Immunotherapy, Adoptive In Vitro Techniques Interleukin-2 - pharmacology Killer Cells, Natural - immunology Medical sciences NK‐92 acute lymphoblastic leukaemia cytotoxicity PI‐3 kinase TNF Phosphatidylinositol 3-Kinases - metabolism Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - enzymology Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - immunology Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - pathology Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - therapy Signal Transduction Transfusions. Complications. Transfusion reactions. Cell and gene therapy Tumor Cells, Cultured Tumor Necrosis Factor-alpha - metabolism Tumor Necrosis Factor-alpha - pharmacology |
| title | Differential killing of pre‐B acute lymphoblastic leukaemia cells by activated NK cells and the NK‐92 ci cell line |
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