Fas (CD95)-related apoptosis and rheumatoid arthritis
Abnormal proliferation and/or persistence of synoviocytes and inflammatory cells has long been described in inflammatory arthritis conditions, but only relatively recently has substantial attention been drawn to the relevance of abnormal apoptotic processes in disease pathogenesis and treatment. Thi...
Gespeichert in:
| Veröffentlicht in: | Rheumatology (Oxford, England) England), 2006-01, Vol.45 (1), p.26-30 |
|---|---|
| 1. Verfasser: | |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 30 |
|---|---|
| container_issue | 1 |
| container_start_page | 26 |
| container_title | Rheumatology (Oxford, England) |
| container_volume | 45 |
| creator | PENG, S. L |
| description | Abnormal proliferation and/or persistence of synoviocytes and inflammatory cells has long been described in inflammatory arthritis conditions, but only relatively recently has substantial attention been drawn to the relevance of abnormal apoptotic processes in disease pathogenesis and treatment. This review summarizes a current understanding of the Fas (CD95)–Fas ligand (CD178) apoptotic system, which has most predominantly been examined in rheumatoid arthritis. There, synovial inflammation is often characterized by a unique resistance to Fas-related apoptosis, and agonistic therapeutic interventions upon Fas have consistently been found beneficial in both animal and human disease models. Therefore, modulation of the Fas pathway will hopefully be of both pathogenic and therapeutic interest in the study of inflammatory arthritis conditions in general. |
| doi_str_mv | 10.1093/rheumatology/kei113 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67582523</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>946387431</sourcerecordid><originalsourceid>FETCH-LOGICAL-c540t-a4b2d4f9a8813ca6ac82ec3f7c86ffaf823981bfeac566fa7da0a81c97890e1f3</originalsourceid><addsrcrecordid>eNqFkFtPGzEQha2qqNz6CypVUSUQPCx47PXtEcIlSAgemqpVX6yJ1y6GTTbYuxL8ezZKCKgvPM1I850zOoeQb0CPgBp-nO58N8W2qZt_z8cPPgLwT2QLSskKyjn7vN5ZuUm2c76nlArg-gvZBAnCmFJuEXGBeXAwPDPisEi-xtZXA5w387bJMQ9wVg1e38T-kNq7FNuYd8lGwDr7r6u5Q35dnI-Ho-L69vJqeHJdOFHStsBywqoyGNQauEOJTjPveFBOyxAwaMaNhknw6ISUAVWFFDU4o7ShHgLfIftL33lqHjufWzuN2fm6xplvumylEpoJxj8EGdV9YAo9-OM_8L7p0qwPYcEIKRSohRtfQi41OScf7DzFKaZnC9Quurfvu7fL7nvV95V1N5n66k2zKrsH9lYAZod1SDhzMb9xqmQK9MKoWHIxt_5pfcf00AfmStjRn79W8d-n45vxT3vJXwBiLZ-S</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>195657173</pqid></control><display><type>article</type><title>Fas (CD95)-related apoptosis and rheumatoid arthritis</title><source>MEDLINE</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Alma/SFX Local Collection</source><creator>PENG, S. L</creator><creatorcontrib>PENG, S. L</creatorcontrib><description>Abnormal proliferation and/or persistence of synoviocytes and inflammatory cells has long been described in inflammatory arthritis conditions, but only relatively recently has substantial attention been drawn to the relevance of abnormal apoptotic processes in disease pathogenesis and treatment. This review summarizes a current understanding of the Fas (CD95)–Fas ligand (CD178) apoptotic system, which has most predominantly been examined in rheumatoid arthritis. There, synovial inflammation is often characterized by a unique resistance to Fas-related apoptosis, and agonistic therapeutic interventions upon Fas have consistently been found beneficial in both animal and human disease models. Therefore, modulation of the Fas pathway will hopefully be of both pathogenic and therapeutic interest in the study of inflammatory arthritis conditions in general.</description><identifier>ISSN: 1462-0324</identifier><identifier>EISSN: 1462-0332</identifier><identifier>DOI: 10.1093/rheumatology/kei113</identifier><identifier>PMID: 16159946</identifier><identifier>CODEN: BJRHDF</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animals ; Apoptosis - immunology ; Arthritis, Rheumatoid - immunology ; Arthritis, Rheumatoid - therapy ; Biological and medical sciences ; Cytokines - immunology ; Diseases of the osteoarticular system ; Fas Ligand Protein ; fas Receptor - physiology ; Humans ; Inflammatory joint diseases ; Medical sciences ; Membrane Glycoproteins - physiology ; Models, Animal ; Synovial Membrane - immunology ; Tumor Necrosis Factors - physiology</subject><ispartof>Rheumatology (Oxford, England), 2006-01, Vol.45 (1), p.26-30</ispartof><rights>2006 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Jan 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-a4b2d4f9a8813ca6ac82ec3f7c86ffaf823981bfeac566fa7da0a81c97890e1f3</citedby><cites>FETCH-LOGICAL-c540t-a4b2d4f9a8813ca6ac82ec3f7c86ffaf823981bfeac566fa7da0a81c97890e1f3</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=17427183$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16159946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>PENG, S. L</creatorcontrib><title>Fas (CD95)-related apoptosis and rheumatoid arthritis</title><title>Rheumatology (Oxford, England)</title><addtitle>Rheumatology</addtitle><description>Abnormal proliferation and/or persistence of synoviocytes and inflammatory cells has long been described in inflammatory arthritis conditions, but only relatively recently has substantial attention been drawn to the relevance of abnormal apoptotic processes in disease pathogenesis and treatment. This review summarizes a current understanding of the Fas (CD95)–Fas ligand (CD178) apoptotic system, which has most predominantly been examined in rheumatoid arthritis. There, synovial inflammation is often characterized by a unique resistance to Fas-related apoptosis, and agonistic therapeutic interventions upon Fas have consistently been found beneficial in both animal and human disease models. Therefore, modulation of the Fas pathway will hopefully be of both pathogenic and therapeutic interest in the study of inflammatory arthritis conditions in general.</description><subject>Animals</subject><subject>Apoptosis - immunology</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - therapy</subject><subject>Biological and medical sciences</subject><subject>Cytokines - immunology</subject><subject>Diseases of the osteoarticular system</subject><subject>Fas Ligand Protein</subject><subject>fas Receptor - physiology</subject><subject>Humans</subject><subject>Inflammatory joint diseases</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - physiology</subject><subject>Models, Animal</subject><subject>Synovial Membrane - immunology</subject><subject>Tumor Necrosis Factors - physiology</subject><issn>1462-0324</issn><issn>1462-0332</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkFtPGzEQha2qqNz6CypVUSUQPCx47PXtEcIlSAgemqpVX6yJ1y6GTTbYuxL8ezZKCKgvPM1I850zOoeQb0CPgBp-nO58N8W2qZt_z8cPPgLwT2QLSskKyjn7vN5ZuUm2c76nlArg-gvZBAnCmFJuEXGBeXAwPDPisEi-xtZXA5w387bJMQ9wVg1e38T-kNq7FNuYd8lGwDr7r6u5Q35dnI-Ho-L69vJqeHJdOFHStsBywqoyGNQauEOJTjPveFBOyxAwaMaNhknw6ISUAVWFFDU4o7ShHgLfIftL33lqHjufWzuN2fm6xplvumylEpoJxj8EGdV9YAo9-OM_8L7p0qwPYcEIKRSohRtfQi41OScf7DzFKaZnC9Quurfvu7fL7nvV95V1N5n66k2zKrsH9lYAZod1SDhzMb9xqmQK9MKoWHIxt_5pfcf00AfmStjRn79W8d-n45vxT3vJXwBiLZ-S</recordid><startdate>20060101</startdate><enddate>20060101</enddate><creator>PENG, S. L</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><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>7QP</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20060101</creationdate><title>Fas (CD95)-related apoptosis and rheumatoid arthritis</title><author>PENG, S. L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-a4b2d4f9a8813ca6ac82ec3f7c86ffaf823981bfeac566fa7da0a81c97890e1f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Apoptosis - immunology</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Arthritis, Rheumatoid - therapy</topic><topic>Biological and medical sciences</topic><topic>Cytokines - immunology</topic><topic>Diseases of the osteoarticular system</topic><topic>Fas Ligand Protein</topic><topic>fas Receptor - physiology</topic><topic>Humans</topic><topic>Inflammatory joint diseases</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - physiology</topic><topic>Models, Animal</topic><topic>Synovial Membrane - immunology</topic><topic>Tumor Necrosis Factors - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>PENG, S. L</creatorcontrib><collection>Istex</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Rheumatology (Oxford, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>PENG, S. L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fas (CD95)-related apoptosis and rheumatoid arthritis</atitle><jtitle>Rheumatology (Oxford, England)</jtitle><addtitle>Rheumatology</addtitle><date>2006-01-01</date><risdate>2006</risdate><volume>45</volume><issue>1</issue><spage>26</spage><epage>30</epage><pages>26-30</pages><issn>1462-0324</issn><eissn>1462-0332</eissn><coden>BJRHDF</coden><abstract>Abnormal proliferation and/or persistence of synoviocytes and inflammatory cells has long been described in inflammatory arthritis conditions, but only relatively recently has substantial attention been drawn to the relevance of abnormal apoptotic processes in disease pathogenesis and treatment. This review summarizes a current understanding of the Fas (CD95)–Fas ligand (CD178) apoptotic system, which has most predominantly been examined in rheumatoid arthritis. There, synovial inflammation is often characterized by a unique resistance to Fas-related apoptosis, and agonistic therapeutic interventions upon Fas have consistently been found beneficial in both animal and human disease models. Therefore, modulation of the Fas pathway will hopefully be of both pathogenic and therapeutic interest in the study of inflammatory arthritis conditions in general.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>16159946</pmid><doi>10.1093/rheumatology/kei113</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1462-0324 |
| ispartof | Rheumatology (Oxford, England), 2006-01, Vol.45 (1), p.26-30 |
| issn | 1462-0324 1462-0332 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67582523 |
| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Animals Apoptosis - immunology Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - therapy Biological and medical sciences Cytokines - immunology Diseases of the osteoarticular system Fas Ligand Protein fas Receptor - physiology Humans Inflammatory joint diseases Medical sciences Membrane Glycoproteins - physiology Models, Animal Synovial Membrane - immunology Tumor Necrosis Factors - physiology |
| title | Fas (CD95)-related apoptosis and rheumatoid arthritis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-22T11%3A24%3A04IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Fas%20(CD95)-related%20apoptosis%20and%20rheumatoid%20arthritis&rft.jtitle=Rheumatology%20(Oxford,%20England)&rft.au=PENG,%20S.%20L&rft.date=2006-01-01&rft.volume=45&rft.issue=1&rft.spage=26&rft.epage=30&rft.pages=26-30&rft.issn=1462-0324&rft.eissn=1462-0332&rft.coden=BJRHDF&rft_id=info:doi/10.1093/rheumatology/kei113&rft_dat=%3Cproquest_cross%3E946387431%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=195657173&rft_id=info:pmid/16159946&rfr_iscdi=true |