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Synovial fibroblasts as accessory cells for staphylococcal enterotoxin-mediated T-cell activation
Rheumatoid arthritis (RA) is thought to be the result of T-cell-mediated autoimmune phenomena. So far, a critical autoantigen has not been identified. Recently, superantigens have been implied in the pathogenesis of RA. In the present study it was tested whether major histocompatibility complex (MHC...
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Published in: | Immunology 1995-07, Vol.85 (3), p.461-466 |
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creator | Kraft, M Filsinger, S Krämer, K L Kabelitz, D Hänsch, G M Schoels, M |
description | Rheumatoid arthritis (RA) is thought to be the result of T-cell-mediated autoimmune phenomena. So far, a critical autoantigen has not been identified. Recently, superantigens have been implied in the pathogenesis of RA. In the present study it was tested whether major histocompatibility complex (MHC) class II-positive synovial fibroblast cells (SFC) function as superantigen-presenting cells. SFC were stimulated with interferon-gamma (IFN-gamma) to express class II antigens; then they were cultivated in the presence of T cells with or without staphylococcal enterotoxins (SE). T-cell activation was measured as proliferation and interleukin-2 (IL-2) production. Depending on the dose and type of SE, activation of T-cell clones and also of peripheral T cells was seen. T-cell activation was inhibited by antibodies to MHC class II antigens and also by antibodies to intracellular adhesion molecule type-1 (ICAM-1). The data suggest that class II-positive SFC have the capacity to serve as accessory cells for superantigen-mediated T-cell activation. Thus SFC may participate in the propagation of a T-cell dependent immune response. |
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So far, a critical autoantigen has not been identified. Recently, superantigens have been implied in the pathogenesis of RA. In the present study it was tested whether major histocompatibility complex (MHC) class II-positive synovial fibroblast cells (SFC) function as superantigen-presenting cells. SFC were stimulated with interferon-gamma (IFN-gamma) to express class II antigens; then they were cultivated in the presence of T cells with or without staphylococcal enterotoxins (SE). T-cell activation was measured as proliferation and interleukin-2 (IL-2) production. Depending on the dose and type of SE, activation of T-cell clones and also of peripheral T cells was seen. T-cell activation was inhibited by antibodies to MHC class II antigens and also by antibodies to intracellular adhesion molecule type-1 (ICAM-1). The data suggest that class II-positive SFC have the capacity to serve as accessory cells for superantigen-mediated T-cell activation. Thus SFC may participate in the propagation of a T-cell dependent immune response.</description><identifier>ISSN: 0019-2805</identifier><identifier>EISSN: 1365-2567</identifier><identifier>PMID: 7558136</identifier><language>eng</language><publisher>England</publisher><subject>Antigen-Presenting Cells - immunology ; Arthritis, Rheumatoid - immunology ; Cell Division - immunology ; Cells, Cultured ; Clone Cells - immunology ; Enterotoxins - immunology ; Fibroblasts - immunology ; HLA-D Antigens - analysis ; Humans ; Intercellular Adhesion Molecule-1 - immunology ; Interleukin-2 - biosynthesis ; Lymphocyte Activation - immunology ; Staphylococcus ; Staphylococcus aureus - immunology ; Superantigens - immunology ; Synovial Membrane - immunology ; T-Lymphocytes - immunology</subject><ispartof>Immunology, 1995-07, Vol.85 (3), p.461-466</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1383921/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1383921/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7558136$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kraft, M</creatorcontrib><creatorcontrib>Filsinger, S</creatorcontrib><creatorcontrib>Krämer, K L</creatorcontrib><creatorcontrib>Kabelitz, D</creatorcontrib><creatorcontrib>Hänsch, G M</creatorcontrib><creatorcontrib>Schoels, M</creatorcontrib><title>Synovial fibroblasts as accessory cells for staphylococcal enterotoxin-mediated T-cell activation</title><title>Immunology</title><addtitle>Immunology</addtitle><description>Rheumatoid arthritis (RA) is thought to be the result of T-cell-mediated autoimmune phenomena. So far, a critical autoantigen has not been identified. Recently, superantigens have been implied in the pathogenesis of RA. In the present study it was tested whether major histocompatibility complex (MHC) class II-positive synovial fibroblast cells (SFC) function as superantigen-presenting cells. SFC were stimulated with interferon-gamma (IFN-gamma) to express class II antigens; then they were cultivated in the presence of T cells with or without staphylococcal enterotoxins (SE). T-cell activation was measured as proliferation and interleukin-2 (IL-2) production. Depending on the dose and type of SE, activation of T-cell clones and also of peripheral T cells was seen. T-cell activation was inhibited by antibodies to MHC class II antigens and also by antibodies to intracellular adhesion molecule type-1 (ICAM-1). The data suggest that class II-positive SFC have the capacity to serve as accessory cells for superantigen-mediated T-cell activation. Thus SFC may participate in the propagation of a T-cell dependent immune response.</description><subject>Antigen-Presenting Cells - immunology</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Cell Division - immunology</subject><subject>Cells, Cultured</subject><subject>Clone Cells - immunology</subject><subject>Enterotoxins - immunology</subject><subject>Fibroblasts - immunology</subject><subject>HLA-D Antigens - analysis</subject><subject>Humans</subject><subject>Intercellular Adhesion Molecule-1 - immunology</subject><subject>Interleukin-2 - biosynthesis</subject><subject>Lymphocyte Activation - immunology</subject><subject>Staphylococcus</subject><subject>Staphylococcus aureus - immunology</subject><subject>Superantigens - immunology</subject><subject>Synovial Membrane - immunology</subject><subject>T-Lymphocytes - immunology</subject><issn>0019-2805</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><recordid>eNqFkE1LAzEQhoMotVZ_grAnbwv52CSbiyBFrVDwYD2H2TRrI9vNmqTF_femWERPwsDMMM-8vDMnaEqY4CXlQp6iKcZElbTG_BxdxPieW4Y5n6CJ5LzO4BTBy9j7vYOuaF0TfNNBTLGAHMbYGH0YC2O7LhatD0VMMGzGzhtvTN6wfbLBJ__p-nJr1w6SXRer8sDn9eT2kJzvL9FZC120V8c8Q68P96v5olw-Pz7N75blQGmVygoYsVxSQUzFRAOtzZWQQtqqMVJh1mAAhRVribKEV0a1Zm1MzW2DhZCYzdDtt-6wa7Ibk90F6PQQ3BbCqD04_XfSu41-83tNWM0UJVng5igQ_MfOxqS3Lh6Ogd76XdRScoprKf4FiagZrnCdwevfln68HL_PvgA-pYUJ</recordid><startdate>19950701</startdate><enddate>19950701</enddate><creator>Kraft, M</creator><creator>Filsinger, S</creator><creator>Krämer, K L</creator><creator>Kabelitz, D</creator><creator>Hänsch, G M</creator><creator>Schoels, M</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19950701</creationdate><title>Synovial fibroblasts as accessory cells for staphylococcal enterotoxin-mediated T-cell activation</title><author>Kraft, M ; Filsinger, S ; Krämer, K L ; Kabelitz, D ; Hänsch, G M ; Schoels, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p224t-4a31e57261c436bafe61c6767e4bc7903b0aa9093f19e154c9fcdcc85eb066703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Antigen-Presenting Cells - immunology</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Cell Division - immunology</topic><topic>Cells, Cultured</topic><topic>Clone Cells - immunology</topic><topic>Enterotoxins - immunology</topic><topic>Fibroblasts - immunology</topic><topic>HLA-D Antigens - analysis</topic><topic>Humans</topic><topic>Intercellular Adhesion Molecule-1 - immunology</topic><topic>Interleukin-2 - biosynthesis</topic><topic>Lymphocyte Activation - immunology</topic><topic>Staphylococcus</topic><topic>Staphylococcus aureus - immunology</topic><topic>Superantigens - immunology</topic><topic>Synovial Membrane - immunology</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kraft, M</creatorcontrib><creatorcontrib>Filsinger, S</creatorcontrib><creatorcontrib>Krämer, K L</creatorcontrib><creatorcontrib>Kabelitz, D</creatorcontrib><creatorcontrib>Hänsch, G M</creatorcontrib><creatorcontrib>Schoels, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kraft, M</au><au>Filsinger, S</au><au>Krämer, K L</au><au>Kabelitz, D</au><au>Hänsch, G M</au><au>Schoels, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synovial fibroblasts as accessory cells for staphylococcal enterotoxin-mediated T-cell activation</atitle><jtitle>Immunology</jtitle><addtitle>Immunology</addtitle><date>1995-07-01</date><risdate>1995</risdate><volume>85</volume><issue>3</issue><spage>461</spage><epage>466</epage><pages>461-466</pages><issn>0019-2805</issn><eissn>1365-2567</eissn><abstract>Rheumatoid arthritis (RA) is thought to be the result of T-cell-mediated autoimmune phenomena. So far, a critical autoantigen has not been identified. Recently, superantigens have been implied in the pathogenesis of RA. In the present study it was tested whether major histocompatibility complex (MHC) class II-positive synovial fibroblast cells (SFC) function as superantigen-presenting cells. SFC were stimulated with interferon-gamma (IFN-gamma) to express class II antigens; then they were cultivated in the presence of T cells with or without staphylococcal enterotoxins (SE). T-cell activation was measured as proliferation and interleukin-2 (IL-2) production. Depending on the dose and type of SE, activation of T-cell clones and also of peripheral T cells was seen. T-cell activation was inhibited by antibodies to MHC class II antigens and also by antibodies to intracellular adhesion molecule type-1 (ICAM-1). The data suggest that class II-positive SFC have the capacity to serve as accessory cells for superantigen-mediated T-cell activation. Thus SFC may participate in the propagation of a T-cell dependent immune response.</abstract><cop>England</cop><pmid>7558136</pmid><tpages>6</tpages></addata></record> |
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subjects | Antigen-Presenting Cells - immunology Arthritis, Rheumatoid - immunology Cell Division - immunology Cells, Cultured Clone Cells - immunology Enterotoxins - immunology Fibroblasts - immunology HLA-D Antigens - analysis Humans Intercellular Adhesion Molecule-1 - immunology Interleukin-2 - biosynthesis Lymphocyte Activation - immunology Staphylococcus Staphylococcus aureus - immunology Superantigens - immunology Synovial Membrane - immunology T-Lymphocytes - immunology |
title | Synovial fibroblasts as accessory cells for staphylococcal enterotoxin-mediated T-cell activation |
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