Chemical Reduction of Oxidized Human Lymphocytes Inhibits Interleukin 2 Production but not Induction of Interleukin 2 Responsiveness
Treatment with neuraminidase (NA) plus galactose oxidase (GalOxase) does not cause stimulation of human thymocytes. However, stimulation can be achieved by addition of exogenous interleukin 2 (IL-2). The IL-2-induced stimulation was inhibited with anti-Tac antibody, indicating that NA/GalOxase-oxidi...
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Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 1984-08, Vol.81 (16), p.5209-5213 |
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creator | Roffman, Ehud Sredni, Benjamin Smolinsky, Aram Wilchek, Meir |
description | Treatment with neuraminidase (NA) plus galactose oxidase (GalOxase) does not cause stimulation of human thymocytes. However, stimulation can be achieved by addition of exogenous interleukin 2 (IL-2). The IL-2-induced stimulation was inhibited with anti-Tac antibody, indicating that NA/GalOxase-oxidized cells can serve as inducers of functional IL-2 receptors on IL-2-responding T cells. The induction of IL-2 receptors by the oxidized cells was not inhibited by subsequent reduction with borohydride, since the cells could still be stimulated with IL-2. The presence of IL-2 receptors was also confirmed by flow cytometry using indirect immunofluorescence. Peripheral blood lymphocytes can be stimulated by NA/GalOxase treatment, and the conditioned medium from this treatment can support the growth of an IL-2-dependent line. This stimulation can be inhibited with borohydride and restored with IL-2. The conditioned medium derived from the borohydride-reduced cells cannot support the growth of the IL-2-dependent line, indicating that borohydride inhibits the oxidation-induced IL-2 production. The results suggest that NA/GalOxase-oxidized sites can be modified chemically without losing the potential to induce IL-2 receptors. |
doi_str_mv | 10.1073/pnas.81.16.5209 |
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However, stimulation can be achieved by addition of exogenous interleukin 2 (IL-2). The IL-2-induced stimulation was inhibited with anti-Tac antibody, indicating that NA/GalOxase-oxidized cells can serve as inducers of functional IL-2 receptors on IL-2-responding T cells. The induction of IL-2 receptors by the oxidized cells was not inhibited by subsequent reduction with borohydride, since the cells could still be stimulated with IL-2. The presence of IL-2 receptors was also confirmed by flow cytometry using indirect immunofluorescence. Peripheral blood lymphocytes can be stimulated by NA/GalOxase treatment, and the conditioned medium from this treatment can support the growth of an IL-2-dependent line. This stimulation can be inhibited with borohydride and restored with IL-2. The conditioned medium derived from the borohydride-reduced cells cannot support the growth of the IL-2-dependent line, indicating that borohydride inhibits the oxidation-induced IL-2 production. The results suggest that NA/GalOxase-oxidized sites can be modified chemically without losing the potential to induce IL-2 receptors.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.81.16.5209</identifier><identifier>PMID: 6382260</identifier><language>eng</language><publisher>United States: National Academy of Sciences of the United States of America</publisher><subject>Antigens ; Borohydrides ; Cell Line ; Cell lines ; Cultured cells ; Flow Cytometry ; Fluorescent Antibody Technique ; Galactose Oxidase - pharmacology ; Humans ; Interleukin-2 - biosynthesis ; Interleukin-2 - physiology ; Interleukins ; Kinetics ; Lymphocytes ; Lymphocytes - drug effects ; Lymphocytes - immunology ; Neuraminidase - pharmacology ; Oxidation ; Oxidation-Reduction ; Receptors ; T lymphocytes ; Thymocytes</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1984-08, Vol.81 (16), p.5209-5213</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-48598f77ed6415c7c61bd34ae6abdfa4d83342d93476031004795c12074d81c53</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/81/16.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/24218$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/24218$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,724,777,781,800,882,27905,27906,53772,53774,57998,58231</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6382260$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Roffman, Ehud</creatorcontrib><creatorcontrib>Sredni, Benjamin</creatorcontrib><creatorcontrib>Smolinsky, Aram</creatorcontrib><creatorcontrib>Wilchek, Meir</creatorcontrib><title>Chemical Reduction of Oxidized Human Lymphocytes Inhibits Interleukin 2 Production but not Induction of Interleukin 2 Responsiveness</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Treatment with neuraminidase (NA) plus galactose oxidase (GalOxase) does not cause stimulation of human thymocytes. However, stimulation can be achieved by addition of exogenous interleukin 2 (IL-2). The IL-2-induced stimulation was inhibited with anti-Tac antibody, indicating that NA/GalOxase-oxidized cells can serve as inducers of functional IL-2 receptors on IL-2-responding T cells. The induction of IL-2 receptors by the oxidized cells was not inhibited by subsequent reduction with borohydride, since the cells could still be stimulated with IL-2. The presence of IL-2 receptors was also confirmed by flow cytometry using indirect immunofluorescence. Peripheral blood lymphocytes can be stimulated by NA/GalOxase treatment, and the conditioned medium from this treatment can support the growth of an IL-2-dependent line. This stimulation can be inhibited with borohydride and restored with IL-2. The conditioned medium derived from the borohydride-reduced cells cannot support the growth of the IL-2-dependent line, indicating that borohydride inhibits the oxidation-induced IL-2 production. The results suggest that NA/GalOxase-oxidized sites can be modified chemically without losing the potential to induce IL-2 receptors.</description><subject>Antigens</subject><subject>Borohydrides</subject><subject>Cell Line</subject><subject>Cell lines</subject><subject>Cultured cells</subject><subject>Flow Cytometry</subject><subject>Fluorescent Antibody Technique</subject><subject>Galactose Oxidase - pharmacology</subject><subject>Humans</subject><subject>Interleukin-2 - biosynthesis</subject><subject>Interleukin-2 - physiology</subject><subject>Interleukins</subject><subject>Kinetics</subject><subject>Lymphocytes</subject><subject>Lymphocytes - drug effects</subject><subject>Lymphocytes - immunology</subject><subject>Neuraminidase - pharmacology</subject><subject>Oxidation</subject><subject>Oxidation-Reduction</subject><subject>Receptors</subject><subject>T lymphocytes</subject><subject>Thymocytes</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9r2zAYhsVY6bJu58Fgw6f15FS_LMuHHUbo1kKgo2xnIcufF3W25ElyaXreHz6bpKG57CTB87yvBC9C7wheElyyi8HpuJRkScSyoLh6gRYEVyQXvMIv0QJjWuaSU_4KvY7xDmNcFRKfolPBJKUCL9Df1QZ6a3SX3UIzmmS9y3yb3TzYxj5Ck12NvXbZetsPG2-2CWJ27Ta2tmm-JAgdjL-ty2j2PfinfD2mzPk0Cc8aj-1biIN30d6DgxjfoJNWdxHe7s8z9PPr5Y_VVb6--Xa9-rLODRck5VwWlWzLEhrBSWFKI0jdMK5B6LppNW8kY5w2FeOlwIxgzMuqMITickLEFOwMfd71DmPdQ2PApaA7NQTb67BVXlt1TJzdqF_-XrGKCFFO-U_7fPB_RohJ9TYa6DrtwI9RSUKpFBWbxIudaIKPMUB7eINgNe-m5t0mXxGh5t2mxIfnXzv4-6Em_nHP5-ATPSo4_6-g2rHrEjykyXy_M-9i8uGgUk6JZP8Aoua38Q</recordid><startdate>19840801</startdate><enddate>19840801</enddate><creator>Roffman, Ehud</creator><creator>Sredni, Benjamin</creator><creator>Smolinsky, Aram</creator><creator>Wilchek, Meir</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><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>19840801</creationdate><title>Chemical Reduction of Oxidized Human Lymphocytes Inhibits Interleukin 2 Production but not Induction of Interleukin 2 Responsiveness</title><author>Roffman, Ehud ; Sredni, Benjamin ; Smolinsky, Aram ; Wilchek, Meir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-48598f77ed6415c7c61bd34ae6abdfa4d83342d93476031004795c12074d81c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Antigens</topic><topic>Borohydrides</topic><topic>Cell Line</topic><topic>Cell lines</topic><topic>Cultured cells</topic><topic>Flow Cytometry</topic><topic>Fluorescent Antibody Technique</topic><topic>Galactose Oxidase - pharmacology</topic><topic>Humans</topic><topic>Interleukin-2 - biosynthesis</topic><topic>Interleukin-2 - physiology</topic><topic>Interleukins</topic><topic>Kinetics</topic><topic>Lymphocytes</topic><topic>Lymphocytes - drug effects</topic><topic>Lymphocytes - immunology</topic><topic>Neuraminidase - pharmacology</topic><topic>Oxidation</topic><topic>Oxidation-Reduction</topic><topic>Receptors</topic><topic>T lymphocytes</topic><topic>Thymocytes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Roffman, Ehud</creatorcontrib><creatorcontrib>Sredni, Benjamin</creatorcontrib><creatorcontrib>Smolinsky, Aram</creatorcontrib><creatorcontrib>Wilchek, Meir</creatorcontrib><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>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Roffman, Ehud</au><au>Sredni, Benjamin</au><au>Smolinsky, Aram</au><au>Wilchek, Meir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chemical Reduction of Oxidized Human Lymphocytes Inhibits Interleukin 2 Production but not Induction of Interleukin 2 Responsiveness</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1984-08-01</date><risdate>1984</risdate><volume>81</volume><issue>16</issue><spage>5209</spage><epage>5213</epage><pages>5209-5213</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Treatment with neuraminidase (NA) plus galactose oxidase (GalOxase) does not cause stimulation of human thymocytes. However, stimulation can be achieved by addition of exogenous interleukin 2 (IL-2). The IL-2-induced stimulation was inhibited with anti-Tac antibody, indicating that NA/GalOxase-oxidized cells can serve as inducers of functional IL-2 receptors on IL-2-responding T cells. The induction of IL-2 receptors by the oxidized cells was not inhibited by subsequent reduction with borohydride, since the cells could still be stimulated with IL-2. The presence of IL-2 receptors was also confirmed by flow cytometry using indirect immunofluorescence. Peripheral blood lymphocytes can be stimulated by NA/GalOxase treatment, and the conditioned medium from this treatment can support the growth of an IL-2-dependent line. This stimulation can be inhibited with borohydride and restored with IL-2. The conditioned medium derived from the borohydride-reduced cells cannot support the growth of the IL-2-dependent line, indicating that borohydride inhibits the oxidation-induced IL-2 production. The results suggest that NA/GalOxase-oxidized sites can be modified chemically without losing the potential to induce IL-2 receptors.</abstract><cop>United States</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>6382260</pmid><doi>10.1073/pnas.81.16.5209</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Antigens Borohydrides Cell Line Cell lines Cultured cells Flow Cytometry Fluorescent Antibody Technique Galactose Oxidase - pharmacology Humans Interleukin-2 - biosynthesis Interleukin-2 - physiology Interleukins Kinetics Lymphocytes Lymphocytes - drug effects Lymphocytes - immunology Neuraminidase - pharmacology Oxidation Oxidation-Reduction Receptors T lymphocytes Thymocytes |
title | Chemical Reduction of Oxidized Human Lymphocytes Inhibits Interleukin 2 Production but not Induction of Interleukin 2 Responsiveness |
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