Targeting cell migration in rheumatoid arthritis
PURPOSE OF REVIEWTo provide an update of past failures, future prospects and key challenges facing the therapeutic targeting of chemokines and their receptors in rheumatoid arthritis. RECENT FINDINGSClinical trials in rheumatoid arthritis have been undertaken with small molecule antagonists or neutr...
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Veröffentlicht in: | Current opinion in rheumatology 2015-03, Vol.27 (2), p.204-211 |
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creator | Asquith, Darren L Bryce, Steven A Nibbs, Robert J.B |
description | PURPOSE OF REVIEWTo provide an update of past failures, future prospects and key challenges facing the therapeutic targeting of chemokines and their receptors in rheumatoid arthritis.
RECENT FINDINGSClinical trials in rheumatoid arthritis have been undertaken with small molecule antagonists or neutralizing antibodies targeting CCR1, CCR5 and CXCL10. Some encouraging results have emerged. Laboratory and clinical research has identified CCL19, CXCL13 and CXCL12, and their receptors, as potential future targets. Developments in our appreciation of posttranslational chemokine modification highlight the complexity of chemokine networks operating in inflamed tissues, and the substantial gaps in existing knowledge.
SUMMARYDespite previous disappointments, there are still reasons to be optimistic that drugs targeting chemokines and their receptors could be developed for the treatment of rheumatoid arthritis. However, a deeper understanding of the chemokine networks at work in inflamed joints is a necessary prerequisite. |
doi_str_mv | 10.1097/BOR.0000000000000150 |
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RECENT FINDINGSClinical trials in rheumatoid arthritis have been undertaken with small molecule antagonists or neutralizing antibodies targeting CCR1, CCR5 and CXCL10. Some encouraging results have emerged. Laboratory and clinical research has identified CCL19, CXCL13 and CXCL12, and their receptors, as potential future targets. Developments in our appreciation of posttranslational chemokine modification highlight the complexity of chemokine networks operating in inflamed tissues, and the substantial gaps in existing knowledge.
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RECENT FINDINGSClinical trials in rheumatoid arthritis have been undertaken with small molecule antagonists or neutralizing antibodies targeting CCR1, CCR5 and CXCL10. Some encouraging results have emerged. Laboratory and clinical research has identified CCL19, CXCL13 and CXCL12, and their receptors, as potential future targets. Developments in our appreciation of posttranslational chemokine modification highlight the complexity of chemokine networks operating in inflamed tissues, and the substantial gaps in existing knowledge.
SUMMARYDespite previous disappointments, there are still reasons to be optimistic that drugs targeting chemokines and their receptors could be developed for the treatment of rheumatoid arthritis. However, a deeper understanding of the chemokine networks at work in inflamed joints is a necessary prerequisite.</description><subject>Antirheumatic Agents - pharmacology</subject><subject>Antirheumatic Agents - therapeutic use</subject><subject>Arthritis, Rheumatoid - drug therapy</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Cell Migration Inhibition - drug effects</subject><subject>Chemokines - antagonists & inhibitors</subject><subject>Chemokines - immunology</subject><subject>Humans</subject><subject>Leukocytes - drug effects</subject><subject>Molecular Targeted Therapy - methods</subject><subject>Molecular Targeted Therapy - trends</subject><subject>Receptors, Chemokine - antagonists & inhibitors</subject><issn>1040-8711</issn><issn>1531-6963</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLAzEUhYMotlb_gcgs3UxNZpJJstTiCwoFqeuQ5tGJzqMmGYr_3pRWERfeu7h38Z1zLweASwSnCHJ6c7d4mcLfhQg8AmNESpRXvCqP0w4xzBlFaATOQnhLSMFRcQpGBalgCUs2BnAp_dpE160zZZoma93ay-j6LnNd5msztDL2TmfSx9q76MI5OLGyCebiMCfg9eF-OXvK54vH59ntPFeYUphbgzhnrCAQU14qiAkqjJZ2BaVmykqjWbVSEluqqa1IwQi3mkilDC01w7ycgOu978b3H4MJUbQu7F6UnemHIFAS4dQcJRTvUeX7ELyxYuNdK_2nQFDsshIpK_E3qyS7OlwYVq3RP6LvcBLA9sC2b6Lx4b0ZtsaL2sgm1v97fwFLHnUE</recordid><startdate>201503</startdate><enddate>201503</enddate><creator>Asquith, Darren L</creator><creator>Bryce, Steven A</creator><creator>Nibbs, Robert J.B</creator><general>Copyright Wolters Kluwer Health, Inc. All rights reserved</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></search><sort><creationdate>201503</creationdate><title>Targeting cell migration in rheumatoid arthritis</title><author>Asquith, Darren L ; Bryce, Steven A ; Nibbs, Robert J.B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4770-fe199882504793c04512edafb0ad8cfaed86bca4f7d7f652859fd5acce73d8493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Antirheumatic Agents - pharmacology</topic><topic>Antirheumatic Agents - therapeutic use</topic><topic>Arthritis, Rheumatoid - drug therapy</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Cell Migration Inhibition - drug effects</topic><topic>Chemokines - antagonists & inhibitors</topic><topic>Chemokines - immunology</topic><topic>Humans</topic><topic>Leukocytes - drug effects</topic><topic>Molecular Targeted Therapy - methods</topic><topic>Molecular Targeted Therapy - trends</topic><topic>Receptors, Chemokine - antagonists & inhibitors</topic><toplevel>online_resources</toplevel><creatorcontrib>Asquith, Darren L</creatorcontrib><creatorcontrib>Bryce, Steven A</creatorcontrib><creatorcontrib>Nibbs, Robert J.B</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><jtitle>Current opinion in rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Asquith, Darren L</au><au>Bryce, Steven A</au><au>Nibbs, Robert J.B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting cell migration in rheumatoid arthritis</atitle><jtitle>Current opinion in rheumatology</jtitle><addtitle>Curr Opin Rheumatol</addtitle><date>2015-03</date><risdate>2015</risdate><volume>27</volume><issue>2</issue><spage>204</spage><epage>211</epage><pages>204-211</pages><issn>1040-8711</issn><eissn>1531-6963</eissn><abstract>PURPOSE OF REVIEWTo provide an update of past failures, future prospects and key challenges facing the therapeutic targeting of chemokines and their receptors in rheumatoid arthritis.
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subjects | Antirheumatic Agents - pharmacology Antirheumatic Agents - therapeutic use Arthritis, Rheumatoid - drug therapy Arthritis, Rheumatoid - immunology Cell Migration Inhibition - drug effects Chemokines - antagonists & inhibitors Chemokines - immunology Humans Leukocytes - drug effects Molecular Targeted Therapy - methods Molecular Targeted Therapy - trends Receptors, Chemokine - antagonists & inhibitors |
title | Targeting cell migration in rheumatoid arthritis |
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