Variant mouse lymphoma cells with modified response to interferon demonstrate enhanced immunogenicity

We have previously developed an experimental model for the xenogenization of malignant lymphoma. From highly tumorigenic S49 mouse lymphoma cells that proliferate in suspension culture (designated T-25), we selected variant clones that grew as an adherent monolayer (designated T-25-Adh) and were non...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Cancer Immunology, Immunotherapy Immunotherapy, 1997-07, Vol.44 (5), p.249-256
Hauptverfasser: MADOR, N, FALK, H, BERGEL, M, PANET, A, HOCHMAN, J
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 256
container_issue 5
container_start_page 249
container_title Cancer Immunology, Immunotherapy
container_volume 44
creator MADOR, N
FALK, H
BERGEL, M
PANET, A
HOCHMAN, J
description We have previously developed an experimental model for the xenogenization of malignant lymphoma. From highly tumorigenic S49 mouse lymphoma cells that proliferate in suspension culture (designated T-25), we selected variant clones that grew as an adherent monolayer (designated T-25-Adh) and were non-tumorigenic in syngeneic mice. Furthermore, priming of syngeneic hosts with T-25-Adh cells protected them against subsequent challenges with the tumorigenic T-25 cells. Several lines of evidence have indicated that antigens of an endogenous mouse mammary tumor virus (MMTV) are involved in the immunogenicity of T-25-Adh cells. Since interferon (IFN) is known to affect retroviral assembly and maturation on the cell membrane, we have studied the effects of IFN on endogenous MMTV-related structures, as well as on the immunogenicity of T-25-Adh cells. We observed that mouse alpha and beta interferons affect the morphogenesis of intracellular MMTV-related precursors in the immunogenic T-25-Adh cells, but not in tumorigenic T-25 cells. From T-25-Adh cells we selected variants that were either high responders or low responders to the above-mentioned interferon effect. The high-response variants were significantly more protective against tumorigenic T-25 cells than the low-response variants. Involvement of MMTV-related antigens in the immune response of the host to T-25-Adh cells was further suggested by immunoelectron-microscopical analysis, demonstrating that antisera from mice, immunized with T-25-Adh cells, interacted specifically with cell-surface MMTV budding particles. These findings indicate a novel method for xenogenization of lymphoma cells by IFN. Since endogenous retroviruses are present in all tissues of the mouse, this approach might be applicable to a wide variety of tumors.
doi_str_mv 10.1007/s002620050380
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11037654</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>79168621</sourcerecordid><originalsourceid>FETCH-LOGICAL-c305t-7e08fb435f876caf982ef1bf988811fd838441ef347a7c0a59518ed4f5db32f3</originalsourceid><addsrcrecordid>eNpVkc2LFDEQxYMo67h69Cj0Qby1Vr466ZPIou7CgpfFa8ikKzuRTjImGWX-e7PsMLinKvJ-vBTvEfKWwkcKoD5VADYxAAlcwzOyoYKzEbSkz8kGuIBRAYiX5FWtv_rCYJ4vyMXMhJJy3hD8aUuwqQ0xHyoO6zHudznaweG61uFvaLuuLMEHXIaCdZ9Tp1oeQmpYPJachgVjf23FNhww7WxynQ0xHlK-xxRcaMfX5IW3a8U3p3lJ7r59vbu6Hm9_fL-5-nI7Og6yjQpB-63g0ms1OetnzdDTbZ9aU-oXzbUQFD0XyioHVs6SalyEl8uWM88vyedH2_1hG3FxmPpVq9mXEG05mmyDeaqksDP3-Y-hFLiapOgOH04OJf8-YG0mhvqQhU3YAzJqppOeGO3g-Ai6kmst6M-_UDAPvZgnvXT-3f-nnelTEV1_f9JtdXb1pccY6hljSoKgnP8DlwGYag</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>79168621</pqid></control><display><type>article</type><title>Variant mouse lymphoma cells with modified response to interferon demonstrate enhanced immunogenicity</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><source>PubMed Central</source><creator>MADOR, N ; FALK, H ; BERGEL, M ; PANET, A ; HOCHMAN, J</creator><creatorcontrib>MADOR, N ; FALK, H ; BERGEL, M ; PANET, A ; HOCHMAN, J</creatorcontrib><description>We have previously developed an experimental model for the xenogenization of malignant lymphoma. From highly tumorigenic S49 mouse lymphoma cells that proliferate in suspension culture (designated T-25), we selected variant clones that grew as an adherent monolayer (designated T-25-Adh) and were non-tumorigenic in syngeneic mice. Furthermore, priming of syngeneic hosts with T-25-Adh cells protected them against subsequent challenges with the tumorigenic T-25 cells. Several lines of evidence have indicated that antigens of an endogenous mouse mammary tumor virus (MMTV) are involved in the immunogenicity of T-25-Adh cells. Since interferon (IFN) is known to affect retroviral assembly and maturation on the cell membrane, we have studied the effects of IFN on endogenous MMTV-related structures, as well as on the immunogenicity of T-25-Adh cells. We observed that mouse alpha and beta interferons affect the morphogenesis of intracellular MMTV-related precursors in the immunogenic T-25-Adh cells, but not in tumorigenic T-25 cells. From T-25-Adh cells we selected variants that were either high responders or low responders to the above-mentioned interferon effect. The high-response variants were significantly more protective against tumorigenic T-25 cells than the low-response variants. Involvement of MMTV-related antigens in the immune response of the host to T-25-Adh cells was further suggested by immunoelectron-microscopical analysis, demonstrating that antisera from mice, immunized with T-25-Adh cells, interacted specifically with cell-surface MMTV budding particles. These findings indicate a novel method for xenogenization of lymphoma cells by IFN. Since endogenous retroviruses are present in all tissues of the mouse, this approach might be applicable to a wide variety of tumors.</description><identifier>ISSN: 0340-7004</identifier><identifier>EISSN: 1432-0851</identifier><identifier>DOI: 10.1007/s002620050380</identifier><identifier>PMID: 9247559</identifier><identifier>CODEN: CIIMDN</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Animals ; Antigenic Variation ; Biological and medical sciences ; Cancer Vaccines - genetics ; Cancer Vaccines - immunology ; Host-tumor relations. Immunology. Biological markers ; Interferons - pharmacology ; Lymphoma - genetics ; Lymphoma - immunology ; Lymphoma - prevention &amp; control ; Male ; Mammary Tumor Virus, Mouse - drug effects ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Original ; Transplantation, Isogeneic ; Tumors ; Vaccines, Attenuated</subject><ispartof>Cancer Immunology, Immunotherapy, 1997-07, Vol.44 (5), p.249-256</ispartof><rights>1997 INIST-CNRS</rights><rights>Springer-Verlag Berlin Heidelberg 1997</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c305t-7e08fb435f876caf982ef1bf988811fd838441ef347a7c0a59518ed4f5db32f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11037654/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11037654/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=2750413$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9247559$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MADOR, N</creatorcontrib><creatorcontrib>FALK, H</creatorcontrib><creatorcontrib>BERGEL, M</creatorcontrib><creatorcontrib>PANET, A</creatorcontrib><creatorcontrib>HOCHMAN, J</creatorcontrib><title>Variant mouse lymphoma cells with modified response to interferon demonstrate enhanced immunogenicity</title><title>Cancer Immunology, Immunotherapy</title><addtitle>Cancer Immunol Immunother</addtitle><description>We have previously developed an experimental model for the xenogenization of malignant lymphoma. From highly tumorigenic S49 mouse lymphoma cells that proliferate in suspension culture (designated T-25), we selected variant clones that grew as an adherent monolayer (designated T-25-Adh) and were non-tumorigenic in syngeneic mice. Furthermore, priming of syngeneic hosts with T-25-Adh cells protected them against subsequent challenges with the tumorigenic T-25 cells. Several lines of evidence have indicated that antigens of an endogenous mouse mammary tumor virus (MMTV) are involved in the immunogenicity of T-25-Adh cells. Since interferon (IFN) is known to affect retroviral assembly and maturation on the cell membrane, we have studied the effects of IFN on endogenous MMTV-related structures, as well as on the immunogenicity of T-25-Adh cells. We observed that mouse alpha and beta interferons affect the morphogenesis of intracellular MMTV-related precursors in the immunogenic T-25-Adh cells, but not in tumorigenic T-25 cells. From T-25-Adh cells we selected variants that were either high responders or low responders to the above-mentioned interferon effect. The high-response variants were significantly more protective against tumorigenic T-25 cells than the low-response variants. Involvement of MMTV-related antigens in the immune response of the host to T-25-Adh cells was further suggested by immunoelectron-microscopical analysis, demonstrating that antisera from mice, immunized with T-25-Adh cells, interacted specifically with cell-surface MMTV budding particles. These findings indicate a novel method for xenogenization of lymphoma cells by IFN. Since endogenous retroviruses are present in all tissues of the mouse, this approach might be applicable to a wide variety of tumors.</description><subject>Animals</subject><subject>Antigenic Variation</subject><subject>Biological and medical sciences</subject><subject>Cancer Vaccines - genetics</subject><subject>Cancer Vaccines - immunology</subject><subject>Host-tumor relations. Immunology. Biological markers</subject><subject>Interferons - pharmacology</subject><subject>Lymphoma - genetics</subject><subject>Lymphoma - immunology</subject><subject>Lymphoma - prevention &amp; control</subject><subject>Male</subject><subject>Mammary Tumor Virus, Mouse - drug effects</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Original</subject><subject>Transplantation, Isogeneic</subject><subject>Tumors</subject><subject>Vaccines, Attenuated</subject><issn>0340-7004</issn><issn>1432-0851</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc2LFDEQxYMo67h69Cj0Qby1Vr466ZPIou7CgpfFa8ikKzuRTjImGWX-e7PsMLinKvJ-vBTvEfKWwkcKoD5VADYxAAlcwzOyoYKzEbSkz8kGuIBRAYiX5FWtv_rCYJ4vyMXMhJJy3hD8aUuwqQ0xHyoO6zHudznaweG61uFvaLuuLMEHXIaCdZ9Tp1oeQmpYPJachgVjf23FNhww7WxynQ0xHlK-xxRcaMfX5IW3a8U3p3lJ7r59vbu6Hm9_fL-5-nI7Og6yjQpB-63g0ms1OetnzdDTbZ9aU-oXzbUQFD0XyioHVs6SalyEl8uWM88vyedH2_1hG3FxmPpVq9mXEG05mmyDeaqksDP3-Y-hFLiapOgOH04OJf8-YG0mhvqQhU3YAzJqppOeGO3g-Ai6kmst6M-_UDAPvZgnvXT-3f-nnelTEV1_f9JtdXb1pccY6hljSoKgnP8DlwGYag</recordid><startdate>19970701</startdate><enddate>19970701</enddate><creator>MADOR, N</creator><creator>FALK, H</creator><creator>BERGEL, M</creator><creator>PANET, A</creator><creator>HOCHMAN, J</creator><general>Springer</general><general>Springer-Verlag</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>19970701</creationdate><title>Variant mouse lymphoma cells with modified response to interferon demonstrate enhanced immunogenicity</title><author>MADOR, N ; FALK, H ; BERGEL, M ; PANET, A ; HOCHMAN, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c305t-7e08fb435f876caf982ef1bf988811fd838441ef347a7c0a59518ed4f5db32f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Antigenic Variation</topic><topic>Biological and medical sciences</topic><topic>Cancer Vaccines - genetics</topic><topic>Cancer Vaccines - immunology</topic><topic>Host-tumor relations. Immunology. Biological markers</topic><topic>Interferons - pharmacology</topic><topic>Lymphoma - genetics</topic><topic>Lymphoma - immunology</topic><topic>Lymphoma - prevention &amp; control</topic><topic>Male</topic><topic>Mammary Tumor Virus, Mouse - drug effects</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Original</topic><topic>Transplantation, Isogeneic</topic><topic>Tumors</topic><topic>Vaccines, Attenuated</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MADOR, N</creatorcontrib><creatorcontrib>FALK, H</creatorcontrib><creatorcontrib>BERGEL, M</creatorcontrib><creatorcontrib>PANET, A</creatorcontrib><creatorcontrib>HOCHMAN, J</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer Immunology, Immunotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MADOR, N</au><au>FALK, H</au><au>BERGEL, M</au><au>PANET, A</au><au>HOCHMAN, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Variant mouse lymphoma cells with modified response to interferon demonstrate enhanced immunogenicity</atitle><jtitle>Cancer Immunology, Immunotherapy</jtitle><addtitle>Cancer Immunol Immunother</addtitle><date>1997-07-01</date><risdate>1997</risdate><volume>44</volume><issue>5</issue><spage>249</spage><epage>256</epage><pages>249-256</pages><issn>0340-7004</issn><eissn>1432-0851</eissn><coden>CIIMDN</coden><abstract>We have previously developed an experimental model for the xenogenization of malignant lymphoma. From highly tumorigenic S49 mouse lymphoma cells that proliferate in suspension culture (designated T-25), we selected variant clones that grew as an adherent monolayer (designated T-25-Adh) and were non-tumorigenic in syngeneic mice. Furthermore, priming of syngeneic hosts with T-25-Adh cells protected them against subsequent challenges with the tumorigenic T-25 cells. Several lines of evidence have indicated that antigens of an endogenous mouse mammary tumor virus (MMTV) are involved in the immunogenicity of T-25-Adh cells. Since interferon (IFN) is known to affect retroviral assembly and maturation on the cell membrane, we have studied the effects of IFN on endogenous MMTV-related structures, as well as on the immunogenicity of T-25-Adh cells. We observed that mouse alpha and beta interferons affect the morphogenesis of intracellular MMTV-related precursors in the immunogenic T-25-Adh cells, but not in tumorigenic T-25 cells. From T-25-Adh cells we selected variants that were either high responders or low responders to the above-mentioned interferon effect. The high-response variants were significantly more protective against tumorigenic T-25 cells than the low-response variants. Involvement of MMTV-related antigens in the immune response of the host to T-25-Adh cells was further suggested by immunoelectron-microscopical analysis, demonstrating that antisera from mice, immunized with T-25-Adh cells, interacted specifically with cell-surface MMTV budding particles. These findings indicate a novel method for xenogenization of lymphoma cells by IFN. Since endogenous retroviruses are present in all tissues of the mouse, this approach might be applicable to a wide variety of tumors.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>9247559</pmid><doi>10.1007/s002620050380</doi><tpages>8</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0340-7004
ispartof Cancer Immunology, Immunotherapy, 1997-07, Vol.44 (5), p.249-256
issn 0340-7004
1432-0851
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11037654
source MEDLINE; Springer Nature - Complete Springer Journals; PubMed Central
subjects Animals
Antigenic Variation
Biological and medical sciences
Cancer Vaccines - genetics
Cancer Vaccines - immunology
Host-tumor relations. Immunology. Biological markers
Interferons - pharmacology
Lymphoma - genetics
Lymphoma - immunology
Lymphoma - prevention & control
Male
Mammary Tumor Virus, Mouse - drug effects
Medical sciences
Mice
Mice, Inbred BALB C
Original
Transplantation, Isogeneic
Tumors
Vaccines, Attenuated
title Variant mouse lymphoma cells with modified response to interferon demonstrate enhanced immunogenicity
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T19%3A41%3A27IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Variant%20mouse%20lymphoma%20cells%20with%20modified%20response%20to%20interferon%20demonstrate%20enhanced%20immunogenicity&rft.jtitle=Cancer%20Immunology,%20Immunotherapy&rft.au=MADOR,%20N&rft.date=1997-07-01&rft.volume=44&rft.issue=5&rft.spage=249&rft.epage=256&rft.pages=249-256&rft.issn=0340-7004&rft.eissn=1432-0851&rft.coden=CIIMDN&rft_id=info:doi/10.1007/s002620050380&rft_dat=%3Cproquest_pubme%3E79168621%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=79168621&rft_id=info:pmid/9247559&rfr_iscdi=true