Activation-induced cell death in T cell hybridomas is due to apoptosis. Morphologic aspects and DNA fragmentation [published erratum appears in J Immunol 1990 Dec 1;145(11):3945]
Some T cell hybridomas, upon activation via the TCR, rapidly undergo cell death. In this paper, we demonstrate that this activation-induced cell death (AICD) is accompanied by morphologic changes seen at the electron and light microscopy levels. The most striking changes are an extensive condensatio...
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| Veröffentlicht in: | The Journal of immunology (1950) 1990-05, Vol.144 (9), p.3326-3333 |
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| creator | Shi, YF Szalay, MG Paskar, L Sahai, BM Boyer, M Singh, B Green, DR |
| description | Some T cell hybridomas, upon activation via the TCR, rapidly undergo cell death. In this paper, we demonstrate that this activation-induced cell death (AICD) is accompanied by morphologic changes seen at the electron and light microscopy levels. The most striking changes are an extensive condensation of the chromatin and formation of membrane blebs. In addition to the morphologic changes, a significant portion of genomic DNA is broken at an interval of approximately 200 bp, producing a ladder of oligonucleosome-sized fragments after gel electrophoresis. Taken together, these observations indicate that AICD proceeds via apoptosis, or programmed cell death. This is additionally supported by the observation that AICD-associated phenomena are at least partially inhibited by cycloheximide or actinomycin D. Curiously, AICD and its associated DNA fragmentation are completely inhibited by aurintricarboxylic acid, a known nuclease inhibitor. The possible relationship between AICD in vitro, and the negative selection process (wherein selection may proceed via AICD of developing, autoreactive thymocytes) is discussed. |
| doi_str_mv | 10.4049/jimmunol.144.9.3326 |
| format | Article |
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Taken together, these observations indicate that AICD proceeds via apoptosis, or programmed cell death. This is additionally supported by the observation that AICD-associated phenomena are at least partially inhibited by cycloheximide or actinomycin D. Curiously, AICD and its associated DNA fragmentation are completely inhibited by aurintricarboxylic acid, a known nuclease inhibitor. 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Psychology ; Hybridomas - cytology ; Lymphocyte Activation - drug effects ; Microscopy, Electron ; Molecular and cellular biology ; Protein Biosynthesis ; RNA - biosynthesis ; T-Lymphocytes - cytology ; Tetradecanoylphorbol Acetate - pharmacology ; Time Factors</subject><ispartof>The Journal of immunology (1950), 1990-05, Vol.144 (9), p.3326-3333</ispartof><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-d00820abed11a940d3c93a4dded01e274265adfafb59a34d8fbd4b4a210e5843</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5580423$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1691753$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, YF</creatorcontrib><creatorcontrib>Szalay, MG</creatorcontrib><creatorcontrib>Paskar, L</creatorcontrib><creatorcontrib>Sahai, BM</creatorcontrib><creatorcontrib>Boyer, M</creatorcontrib><creatorcontrib>Singh, B</creatorcontrib><creatorcontrib>Green, DR</creatorcontrib><title>Activation-induced cell death in T cell hybridomas is due to apoptosis. Morphologic aspects and DNA fragmentation [published erratum appears in J Immunol 1990 Dec 1;145(11):3945]</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Some T cell hybridomas, upon activation via the TCR, rapidly undergo cell death. In this paper, we demonstrate that this activation-induced cell death (AICD) is accompanied by morphologic changes seen at the electron and light microscopy levels. The most striking changes are an extensive condensation of the chromatin and formation of membrane blebs. In addition to the morphologic changes, a significant portion of genomic DNA is broken at an interval of approximately 200 bp, producing a ladder of oligonucleosome-sized fragments after gel electrophoresis. Taken together, these observations indicate that AICD proceeds via apoptosis, or programmed cell death. This is additionally supported by the observation that AICD-associated phenomena are at least partially inhibited by cycloheximide or actinomycin D. Curiously, AICD and its associated DNA fragmentation are completely inhibited by aurintricarboxylic acid, a known nuclease inhibitor. The possible relationship between AICD in vitro, and the negative selection process (wherein selection may proceed via AICD of developing, autoreactive thymocytes) is discussed.</description><subject>Ageing, cell death</subject><subject>Aurintricarboxylic Acid - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Calcimycin - pharmacology</subject><subject>Cell physiology</subject><subject>Cell Survival - drug effects</subject><subject>Concanavalin A - pharmacology</subject><subject>Cycloheximide - pharmacology</subject><subject>Cyclosporins - pharmacology</subject><subject>Dactinomycin - pharmacology</subject><subject>DNA Damage</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hybridomas - cytology</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Microscopy, Electron</subject><subject>Molecular and cellular biology</subject><subject>Protein Biosynthesis</subject><subject>RNA - biosynthesis</subject><subject>T-Lymphocytes - cytology</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>Time Factors</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkcuO1DAQRS0EGpqBL0BIXiAeiwQ7fqQNq9YMj0EDbHqHkFWxnY5HSRzshNb8Fl9IQprHqlSqW_eq6iD0mJKcE65e3fium_rQ5pTzXOWMFfIO2lAhSCYlkXfRhpCiyGgpy_voQUo3hBBJCn6GzqhUtBRsg37uzOh_wOhDn_neTsZZbFzbYutgbLDv8X7tm9sqehs6SNgnbCeHx4BhCMMYkk85_hTi0IQ2HLzBkAZnxoSht_jy8w7XEQ6d68ffMfjrMFWtT82c5GKEcepmn8FBTEvcR3y1XoWpUgRfOoPpG8rFC0pfvmaKi28P0b0a2uQeneo52r97u7_4kF1_eX91sbvODGflmFlCtgWByllKQXFimVEMuLXOEuqKkhdSgK2hroQCxu22riyvOBSUOLHl7Bw9W22HGL5PLo2682l5BfQuTElTISXjks1CtgpNDClFV-sh-g7iraZEL6D0H1B6BqWVXkDNW09O9lPVOftvZyUzz5-e5pAMtPMLe-PTX5kQW8KLRfZ8lTX-0Bx9dDp10LazKdXH4_G_wF8fjavb</recordid><startdate>19900501</startdate><enddate>19900501</enddate><creator>Shi, YF</creator><creator>Szalay, MG</creator><creator>Paskar, L</creator><creator>Sahai, BM</creator><creator>Boyer, M</creator><creator>Singh, B</creator><creator>Green, DR</creator><general>Am Assoc Immnol</general><general>American Association of Immunologists</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>H94</scope></search><sort><creationdate>19900501</creationdate><title>Activation-induced cell death in T cell hybridomas is due to apoptosis. Morphologic aspects and DNA fragmentation [published erratum appears in J Immunol 1990 Dec 1;145(11):3945]</title><author>Shi, YF ; Szalay, MG ; Paskar, L ; Sahai, BM ; Boyer, M ; Singh, B ; Green, DR</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-d00820abed11a940d3c93a4dded01e274265adfafb59a34d8fbd4b4a210e5843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Ageing, cell death</topic><topic>Aurintricarboxylic Acid - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Calcimycin - pharmacology</topic><topic>Cell physiology</topic><topic>Cell Survival - drug effects</topic><topic>Concanavalin A - pharmacology</topic><topic>Cycloheximide - pharmacology</topic><topic>Cyclosporins - pharmacology</topic><topic>Dactinomycin - pharmacology</topic><topic>DNA Damage</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hybridomas - cytology</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Microscopy, Electron</topic><topic>Molecular and cellular biology</topic><topic>Protein Biosynthesis</topic><topic>RNA - biosynthesis</topic><topic>T-Lymphocytes - cytology</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, YF</creatorcontrib><creatorcontrib>Szalay, MG</creatorcontrib><creatorcontrib>Paskar, L</creatorcontrib><creatorcontrib>Sahai, BM</creatorcontrib><creatorcontrib>Boyer, M</creatorcontrib><creatorcontrib>Singh, B</creatorcontrib><creatorcontrib>Green, DR</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>AIDS and Cancer Research Abstracts</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, YF</au><au>Szalay, MG</au><au>Paskar, L</au><au>Sahai, BM</au><au>Boyer, M</au><au>Singh, B</au><au>Green, DR</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation-induced cell death in T cell hybridomas is due to apoptosis. Morphologic aspects and DNA fragmentation [published erratum appears in J Immunol 1990 Dec 1;145(11):3945]</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>1990-05-01</date><risdate>1990</risdate><volume>144</volume><issue>9</issue><spage>3326</spage><epage>3333</epage><pages>3326-3333</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><coden>JOIMA3</coden><abstract>Some T cell hybridomas, upon activation via the TCR, rapidly undergo cell death. In this paper, we demonstrate that this activation-induced cell death (AICD) is accompanied by morphologic changes seen at the electron and light microscopy levels. The most striking changes are an extensive condensation of the chromatin and formation of membrane blebs. In addition to the morphologic changes, a significant portion of genomic DNA is broken at an interval of approximately 200 bp, producing a ladder of oligonucleosome-sized fragments after gel electrophoresis. Taken together, these observations indicate that AICD proceeds via apoptosis, or programmed cell death. This is additionally supported by the observation that AICD-associated phenomena are at least partially inhibited by cycloheximide or actinomycin D. Curiously, AICD and its associated DNA fragmentation are completely inhibited by aurintricarboxylic acid, a known nuclease inhibitor. The possible relationship between AICD in vitro, and the negative selection process (wherein selection may proceed via AICD of developing, autoreactive thymocytes) is discussed.</abstract><cop>Bethesda, MD</cop><pub>Am Assoc Immnol</pub><pmid>1691753</pmid><doi>10.4049/jimmunol.144.9.3326</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Ageing, cell death Aurintricarboxylic Acid - pharmacology Biological and medical sciences Calcimycin - pharmacology Cell physiology Cell Survival - drug effects Concanavalin A - pharmacology Cycloheximide - pharmacology Cyclosporins - pharmacology Dactinomycin - pharmacology DNA Damage Fundamental and applied biological sciences. Psychology Hybridomas - cytology Lymphocyte Activation - drug effects Microscopy, Electron Molecular and cellular biology Protein Biosynthesis RNA - biosynthesis T-Lymphocytes - cytology Tetradecanoylphorbol Acetate - pharmacology Time Factors |
| title | Activation-induced cell death in T cell hybridomas is due to apoptosis. Morphologic aspects and DNA fragmentation [published erratum appears in J Immunol 1990 Dec 1;145(11):3945] |
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