Cytokine-mediated regulation of monocyte/macrophage cytotoxicity in human immunodeficiency virus-1 infection
Monocyte/macrophage-mediated tumor cytotoxicity was studied in patients infected with human immunodeficiency virus-1 (HIV-1) at various stages [Center for disease control (CDC) classification] of the disease. using the P-815 tumor cell line as target cells, the results demonstrated reduced monocyte/...
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Veröffentlicht in: | Medical microbiology and immunology 1992-11, Vol.181 (5), p.267-281 |
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creator | ROSSOL, S GIANNI, G ROSSOL-VOTH, R GALLATI, H MÜLLER, W. E. G MEYER ZUM BÜSCHENFELDE, K.-H |
description | Monocyte/macrophage-mediated tumor cytotoxicity was studied in patients infected with human immunodeficiency virus-1 (HIV-1) at various stages [Center for disease control (CDC) classification] of the disease. using the P-815 tumor cell line as target cells, the results demonstrated reduced monocyte/macrophage cytotoxicity early in HIV-1-related disease (CDCIII, P < 0.01). This cellular dysfunction sustained during the progression of the disease. Evidence could be presented that neither exogenous application of macrophage-stimulating cytokines (e.g. interferons) nor their endogenous induction in vitro restored monocyte/macrophage cytotoxicity. However, enhanced tumor necrosis factor (TNF)-alpha production, which parallels the observed reduced capacity to lyse P-815 tumor cells, might be the major source for monocyte/macrophage-mediated cell lysis. TNF-alpha-induced cytotoxicity can be inhibited by addition of anti-TNF-alpha. Other experimental models using TNF-sensitive tumor target cells may, therefore, mimic monocyte/macrophage-mediated lysis. Suppression of monocyte/macrophage cytotoxicity in later stages of HIV-1 infection (AIDS-related complex, AIDS) could partly be reverted by treatment with the cyclooxygenase blocker, indomethacin. The responsible arachidonic acid product mediating suppression was found to be prostaglandin E2, suggesting that in addition to the direct viral interference cellular dysfunction is at least in part a result of altered cytokine regulation. |
doi_str_mv | 10.1007/BF00198847 |
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E. G ; MEYER ZUM BÜSCHENFELDE, K.-H</creator><creatorcontrib>ROSSOL, S ; GIANNI, G ; ROSSOL-VOTH, R ; GALLATI, H ; MÜLLER, W. E. G ; MEYER ZUM BÜSCHENFELDE, K.-H</creatorcontrib><description>Monocyte/macrophage-mediated tumor cytotoxicity was studied in patients infected with human immunodeficiency virus-1 (HIV-1) at various stages [Center for disease control (CDC) classification] of the disease. using the P-815 tumor cell line as target cells, the results demonstrated reduced monocyte/macrophage cytotoxicity early in HIV-1-related disease (CDCIII, P < 0.01). This cellular dysfunction sustained during the progression of the disease. Evidence could be presented that neither exogenous application of macrophage-stimulating cytokines (e.g. interferons) nor their endogenous induction in vitro restored monocyte/macrophage cytotoxicity. However, enhanced tumor necrosis factor (TNF)-alpha production, which parallels the observed reduced capacity to lyse P-815 tumor cells, might be the major source for monocyte/macrophage-mediated cell lysis. TNF-alpha-induced cytotoxicity can be inhibited by addition of anti-TNF-alpha. Other experimental models using TNF-sensitive tumor target cells may, therefore, mimic monocyte/macrophage-mediated lysis. Suppression of monocyte/macrophage cytotoxicity in later stages of HIV-1 infection (AIDS-related complex, AIDS) could partly be reverted by treatment with the cyclooxygenase blocker, indomethacin. The responsible arachidonic acid product mediating suppression was found to be prostaglandin E2, suggesting that in addition to the direct viral interference cellular dysfunction is at least in part a result of altered cytokine regulation.</description><identifier>ISSN: 0300-8584</identifier><identifier>EISSN: 1432-1831</identifier><identifier>DOI: 10.1007/BF00198847</identifier><identifier>PMID: 1282202</identifier><identifier>CODEN: MMIYAO</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Adult ; AIDS/HIV ; Biological and medical sciences ; Cells, Cultured ; Cytokines - immunology ; Cytotoxicity, Immunologic ; HIV Infections - immunology ; HIV-1 - immunology ; human immunodeficiency virus 1 ; Humans ; Immunodeficiencies ; Immunodeficiencies. Immunoglobulinopathies ; Immunopathology ; Interferons - immunology ; Interleukins - immunology ; Macrophages - immunology ; Medical sciences ; Middle Aged ; Monocytes - immunology ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha - immunology</subject><ispartof>Medical microbiology and immunology, 1992-11, Vol.181 (5), p.267-281</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c342t-3f77fd07cf2fba4643a663f295d9fac81340ef28f7714dc9db94933709f5f0cf3</citedby><cites>FETCH-LOGICAL-c342t-3f77fd07cf2fba4643a663f295d9fac81340ef28f7714dc9db94933709f5f0cf3</cites></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=4460580$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1282202$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ROSSOL, S</creatorcontrib><creatorcontrib>GIANNI, G</creatorcontrib><creatorcontrib>ROSSOL-VOTH, R</creatorcontrib><creatorcontrib>GALLATI, H</creatorcontrib><creatorcontrib>MÜLLER, W. E. G</creatorcontrib><creatorcontrib>MEYER ZUM BÜSCHENFELDE, K.-H</creatorcontrib><title>Cytokine-mediated regulation of monocyte/macrophage cytotoxicity in human immunodeficiency virus-1 infection</title><title>Medical microbiology and immunology</title><addtitle>Med Microbiol Immunol</addtitle><description>Monocyte/macrophage-mediated tumor cytotoxicity was studied in patients infected with human immunodeficiency virus-1 (HIV-1) at various stages [Center for disease control (CDC) classification] of the disease. using the P-815 tumor cell line as target cells, the results demonstrated reduced monocyte/macrophage cytotoxicity early in HIV-1-related disease (CDCIII, P < 0.01). This cellular dysfunction sustained during the progression of the disease. Evidence could be presented that neither exogenous application of macrophage-stimulating cytokines (e.g. interferons) nor their endogenous induction in vitro restored monocyte/macrophage cytotoxicity. However, enhanced tumor necrosis factor (TNF)-alpha production, which parallels the observed reduced capacity to lyse P-815 tumor cells, might be the major source for monocyte/macrophage-mediated cell lysis. TNF-alpha-induced cytotoxicity can be inhibited by addition of anti-TNF-alpha. Other experimental models using TNF-sensitive tumor target cells may, therefore, mimic monocyte/macrophage-mediated lysis. Suppression of monocyte/macrophage cytotoxicity in later stages of HIV-1 infection (AIDS-related complex, AIDS) could partly be reverted by treatment with the cyclooxygenase blocker, indomethacin. The responsible arachidonic acid product mediating suppression was found to be prostaglandin E2, suggesting that in addition to the direct viral interference cellular dysfunction is at least in part a result of altered cytokine regulation.</description><subject>Adult</subject><subject>AIDS/HIV</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>Cytokines - immunology</subject><subject>Cytotoxicity, Immunologic</subject><subject>HIV Infections - immunology</subject><subject>HIV-1 - immunology</subject><subject>human immunodeficiency virus 1</subject><subject>Humans</subject><subject>Immunodeficiencies</subject><subject>Immunodeficiencies. Immunoglobulinopathies</subject><subject>Immunopathology</subject><subject>Interferons - immunology</subject><subject>Interleukins - immunology</subject><subject>Macrophages - immunology</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Monocytes - immunology</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><issn>0300-8584</issn><issn>1432-1831</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkT1PwzAQhi0EKqWwsCNlQAxIoeePJs4IFQWkSiwwR65jt4bELrGDyL_HUSs6stzp7h69w3MIXWK4wwD59GEBgAvOWX6ExphRkmJO8TEaAwVI-YyzU3Tm_Uek8ozACI0w4YQAGaN63gf3aaxKG1UZEVSVtGrd1SIYZxOnk8ZZJ_ugpo2QrdtuxFolcXbB_RhpQp8Ym2y6RtjENE1nXaV03Csr--TbtJ1PcSS0kkPeOTrRovbqYt8n6H3x-DZ_TpevTy_z-2UqKSMhpTrPdQW51ESvBMsYFVlGNSlmVaGF5JgyUJrwiGFWyaJaFaygNIdCzzRITSfoZpe7bd1Xp3woG-Olqmthlet8mdPoaCj_gTjLikFlBG93YHTgfat0uW1NI9q-xFAOPygPP4jw1T61W0WrB3QnPd6v93fhpah1K6w0_g9jLIMZB_oLvTiPvA</recordid><startdate>19921101</startdate><enddate>19921101</enddate><creator>ROSSOL, S</creator><creator>GIANNI, G</creator><creator>ROSSOL-VOTH, R</creator><creator>GALLATI, H</creator><creator>MÜLLER, W. E. G</creator><creator>MEYER ZUM BÜSCHENFELDE, K.-H</creator><general>Springer</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>7X8</scope></search><sort><creationdate>19921101</creationdate><title>Cytokine-mediated regulation of monocyte/macrophage cytotoxicity in human immunodeficiency virus-1 infection</title><author>ROSSOL, S ; GIANNI, G ; ROSSOL-VOTH, R ; GALLATI, H ; MÜLLER, W. E. G ; MEYER ZUM BÜSCHENFELDE, K.-H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c342t-3f77fd07cf2fba4643a663f295d9fac81340ef28f7714dc9db94933709f5f0cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Adult</topic><topic>AIDS/HIV</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>Cytokines - immunology</topic><topic>Cytotoxicity, Immunologic</topic><topic>HIV Infections - immunology</topic><topic>HIV-1 - immunology</topic><topic>human immunodeficiency virus 1</topic><topic>Humans</topic><topic>Immunodeficiencies</topic><topic>Immunodeficiencies. Immunoglobulinopathies</topic><topic>Immunopathology</topic><topic>Interferons - immunology</topic><topic>Interleukins - immunology</topic><topic>Macrophages - immunology</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Monocytes - immunology</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ROSSOL, S</creatorcontrib><creatorcontrib>GIANNI, G</creatorcontrib><creatorcontrib>ROSSOL-VOTH, R</creatorcontrib><creatorcontrib>GALLATI, H</creatorcontrib><creatorcontrib>MÜLLER, W. E. G</creatorcontrib><creatorcontrib>MEYER ZUM BÜSCHENFELDE, K.-H</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>MEDLINE - Academic</collection><jtitle>Medical microbiology and immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ROSSOL, S</au><au>GIANNI, G</au><au>ROSSOL-VOTH, R</au><au>GALLATI, H</au><au>MÜLLER, W. E. G</au><au>MEYER ZUM BÜSCHENFELDE, K.-H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytokine-mediated regulation of monocyte/macrophage cytotoxicity in human immunodeficiency virus-1 infection</atitle><jtitle>Medical microbiology and immunology</jtitle><addtitle>Med Microbiol Immunol</addtitle><date>1992-11-01</date><risdate>1992</risdate><volume>181</volume><issue>5</issue><spage>267</spage><epage>281</epage><pages>267-281</pages><issn>0300-8584</issn><eissn>1432-1831</eissn><coden>MMIYAO</coden><abstract>Monocyte/macrophage-mediated tumor cytotoxicity was studied in patients infected with human immunodeficiency virus-1 (HIV-1) at various stages [Center for disease control (CDC) classification] of the disease. using the P-815 tumor cell line as target cells, the results demonstrated reduced monocyte/macrophage cytotoxicity early in HIV-1-related disease (CDCIII, P < 0.01). This cellular dysfunction sustained during the progression of the disease. Evidence could be presented that neither exogenous application of macrophage-stimulating cytokines (e.g. interferons) nor their endogenous induction in vitro restored monocyte/macrophage cytotoxicity. However, enhanced tumor necrosis factor (TNF)-alpha production, which parallels the observed reduced capacity to lyse P-815 tumor cells, might be the major source for monocyte/macrophage-mediated cell lysis. TNF-alpha-induced cytotoxicity can be inhibited by addition of anti-TNF-alpha. Other experimental models using TNF-sensitive tumor target cells may, therefore, mimic monocyte/macrophage-mediated lysis. Suppression of monocyte/macrophage cytotoxicity in later stages of HIV-1 infection (AIDS-related complex, AIDS) could partly be reverted by treatment with the cyclooxygenase blocker, indomethacin. The responsible arachidonic acid product mediating suppression was found to be prostaglandin E2, suggesting that in addition to the direct viral interference cellular dysfunction is at least in part a result of altered cytokine regulation.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>1282202</pmid><doi>10.1007/BF00198847</doi><tpages>15</tpages></addata></record> |
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subjects | Adult AIDS/HIV Biological and medical sciences Cells, Cultured Cytokines - immunology Cytotoxicity, Immunologic HIV Infections - immunology HIV-1 - immunology human immunodeficiency virus 1 Humans Immunodeficiencies Immunodeficiencies. Immunoglobulinopathies Immunopathology Interferons - immunology Interleukins - immunology Macrophages - immunology Medical sciences Middle Aged Monocytes - immunology Tumor Cells, Cultured Tumor Necrosis Factor-alpha - immunology |
title | Cytokine-mediated regulation of monocyte/macrophage cytotoxicity in human immunodeficiency virus-1 infection |
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