Possible targeting of G protein coupled receptors to manipulate inflammation in vivo using synthetic and natural ligands
Cyclic AMP elevating Gs protein coupled receptors were considered for a long time to be immunosuppressive. One of these receptors, adenosine A2A receptor, was implicated in a physiological mechanism that down regulates inflammation and protects tissues from excessive immune mediated damage. Targetin...
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| Veröffentlicht in: | Annals of the rheumatic diseases 2003-11, Vol.62 (suppl 2), p.ii22-ii24 |
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| container_end_page | ii24 |
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| container_issue | suppl 2 |
| container_start_page | ii22 |
| container_title | Annals of the rheumatic diseases |
| container_volume | 62 |
| creator | Kinsel, J F Sitkovsky, M V |
| description | Cyclic AMP elevating Gs protein coupled receptors were considered for a long time to be immunosuppressive. One of these receptors, adenosine A2A receptor, was implicated in a physiological mechanism that down regulates inflammation and protects tissues from excessive immune mediated damage. Targeting of these receptors by selective agonists may lead to better protocols of anti-inflammatory treatments. At the same time inhibiting the Gs protein coupled mediated signalling with antagonists could be explored in studies of approaches to enhance inflammation and tissue damage. Enhancement of targeted tissue damage is highly desirable when it is cancerous tissue, while enhancement of inflammatory events might be desirable in the development of new vaccine adjuvants. |
| doi_str_mv | 10.1136/ard.62.suppl_2.ii22 |
| format | Article |
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One of these receptors, adenosine A2A receptor, was implicated in a physiological mechanism that down regulates inflammation and protects tissues from excessive immune mediated damage. Targeting of these receptors by selective agonists may lead to better protocols of anti-inflammatory treatments. At the same time inhibiting the Gs protein coupled mediated signalling with antagonists could be explored in studies of approaches to enhance inflammation and tissue damage. Enhancement of targeted tissue damage is highly desirable when it is cancerous tissue, while enhancement of inflammatory events might be desirable in the development of new vaccine adjuvants.</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/ard.62.suppl_2.ii22</identifier><identifier>PMID: 14532142</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><subject>Adenosine ; Adenosine A2 Receptor Antagonists ; Animals ; Anti-Inflammatory Agents - therapeutic use ; Biological and medical sciences ; Caffeine ; GTP-Binding Protein alpha Subunits, Gs - metabolism ; Humans ; Hypoxia ; Immunomodulators ; immunosuppressive loop ; Inflammation ; Inflammation - drug therapy ; Inflammation - physiopathology ; Ligands ; Medical sciences ; metabolic switch ; Mice ; Pathogens ; Pharmacology. Drug treatments ; Physiology ; Proteins ; Receptor, Adenosine A2A - physiology</subject><ispartof>Annals of the rheumatic diseases, 2003-11, Vol.62 (suppl 2), p.ii22-ii24</ispartof><rights>Copyright 2003 by Annals of the Rheumatic Diseases</rights><rights>2004 INIST-CNRS</rights><rights>Copyright: 2003 Copyright 2003 by Annals of the Rheumatic Diseases</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b536t-262673ece8d098764e860fdda720e5498d491eaffde9f37feb906b02e984a12e3</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/PMC1766756/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1766756/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,309,310,314,727,780,784,789,790,885,23930,23931,25140,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15234932$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14532142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kinsel, J F</creatorcontrib><creatorcontrib>Sitkovsky, M V</creatorcontrib><title>Possible targeting of G protein coupled receptors to manipulate inflammation in vivo using synthetic and natural ligands</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>Cyclic AMP elevating Gs protein coupled receptors were considered for a long time to be immunosuppressive. One of these receptors, adenosine A2A receptor, was implicated in a physiological mechanism that down regulates inflammation and protects tissues from excessive immune mediated damage. Targeting of these receptors by selective agonists may lead to better protocols of anti-inflammatory treatments. At the same time inhibiting the Gs protein coupled mediated signalling with antagonists could be explored in studies of approaches to enhance inflammation and tissue damage. Enhancement of targeted tissue damage is highly desirable when it is cancerous tissue, while enhancement of inflammatory events might be desirable in the development of new vaccine adjuvants.</description><subject>Adenosine</subject><subject>Adenosine A2 Receptor Antagonists</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Caffeine</subject><subject>GTP-Binding Protein alpha Subunits, Gs - metabolism</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Immunomodulators</subject><subject>immunosuppressive loop</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - physiopathology</subject><subject>Ligands</subject><subject>Medical sciences</subject><subject>metabolic switch</subject><subject>Mice</subject><subject>Pathogens</subject><subject>Pharmacology. Drug treatments</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Receptor, Adenosine A2A - physiology</subject><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkU9v1DAQxS0EotuFT4CELCF6y-I_iZ1ckKoVFERVCgKulpNMtl4cO9jOqv32eLWrFjhxskbzm-c38xB6QcmKUi7e6NCvBFvFeZqsYitjGHuEFrQUdcGIII_RghDCi7IR8gSdxrjNJalp_RSd0LLijJZsgW6vfYymtYCTDhtIxm2wH_AFnoJPYBzu_DxZ6HGADqbkQ8TJ41E7M81WJ8DGDVaPo07Gu1zgndl5PMe9Trxz6SZLdli7Hjud5qAttmaTy_gMPRm0jfD8-C7R9_fvvq0_FJefLz6uzy-LtuIiFUwwIXn-u-5JU0tRQi3I0PdaMgJV2dR92VDQw9BDM3A5QNsQ0RIGTV1qyoAv0duD7jS3I_QduJRdqCmYUYc75bVRf3ecuVEbv1NUCiErkQXOjgLB_5ohJjWa2IG12oGfo5KVFJWseQZf_QNu_RxcXi5rSdnUlOWzLxE_UF3Ilw8w3FuhRO1zVTlXJZg65qr2ueapl39u8TBzDDIDr4-Ajp22Q9CuM_GBqxgvG77nigNnYoLb-74OP1W-s6zU1Y-1Ep--smt29UXtt18d-Hbc_pfT3xfX0Vc</recordid><startdate>20031101</startdate><enddate>20031101</enddate><creator>Kinsel, J F</creator><creator>Sitkovsky, M V</creator><general>BMJ Publishing Group Ltd and European League Against Rheumatism</general><general>BMJ</general><general>BMJ Publishing Group LTD</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20031101</creationdate><title>Possible targeting of G protein coupled receptors to manipulate inflammation in vivo using synthetic and natural ligands</title><author>Kinsel, J F ; Sitkovsky, M V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b536t-262673ece8d098764e860fdda720e5498d491eaffde9f37feb906b02e984a12e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adenosine</topic><topic>Adenosine A2 Receptor Antagonists</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Caffeine</topic><topic>GTP-Binding Protein alpha Subunits, Gs - metabolism</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Immunomodulators</topic><topic>immunosuppressive loop</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - physiopathology</topic><topic>Ligands</topic><topic>Medical sciences</topic><topic>metabolic switch</topic><topic>Mice</topic><topic>Pathogens</topic><topic>Pharmacology. 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| ispartof | Annals of the rheumatic diseases, 2003-11, Vol.62 (suppl 2), p.ii22-ii24 |
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| language | eng |
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| subjects | Adenosine Adenosine A2 Receptor Antagonists Animals Anti-Inflammatory Agents - therapeutic use Biological and medical sciences Caffeine GTP-Binding Protein alpha Subunits, Gs - metabolism Humans Hypoxia Immunomodulators immunosuppressive loop Inflammation Inflammation - drug therapy Inflammation - physiopathology Ligands Medical sciences metabolic switch Mice Pathogens Pharmacology. Drug treatments Physiology Proteins Receptor, Adenosine A2A - physiology |
| title | Possible targeting of G protein coupled receptors to manipulate inflammation in vivo using synthetic and natural ligands |
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