A review of JAK–STAT signalling in the pathogenesis of spondyloarthritis and the role of JAK inhibition
Abstract Spondyloarthritis (SpA) comprises a group of chronic inflammatory diseases with overlapping clinical, genetic and pathophysiological features including back pain, peripheral arthritis, psoriasis, enthesitis and dactylitis. Several cytokines are involved in the pathogenesis of SpA, variously...
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| Veröffentlicht in: | Rheumatology (Oxford, England) England), 2022-05, Vol.61 (5), p.1783-1794 |
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| creator | McInnes, Iain B Szekanecz, Zoltán McGonagle, Dennis Maksymowych, Walter P Pfeil, Alexander Lippe, Ralph Song, In-Ho Lertratanakul, Apinya Sornasse, Thierry Biljan, Ana Deodhar, Atul |
| description | Abstract
Spondyloarthritis (SpA) comprises a group of chronic inflammatory diseases with overlapping clinical, genetic and pathophysiological features including back pain, peripheral arthritis, psoriasis, enthesitis and dactylitis. Several cytokines are involved in the pathogenesis of SpA, variously contributing to each clinical manifestation. Many SpA-associated cytokines, including IL-23, IL-17, IL-6, type I/II interferon and tumour necrosis factor signal directly or indirectly via the Janus kinase (JAK)–signal transducer and activator of transcription pathway. JAK signalling also regulates development and maturation of cells of the innate and adaptive immune systems. Accordingly, disruption of this signalling pathway by small molecule oral JAK inhibitors can inhibit signalling implicated in SpA pathogenesis. Herein we discuss the role of JAK signalling in the pathogenesis of SpA and summarize the safety and efficacy of JAK inhibition by reference to relevant SpA clinical trials. |
| doi_str_mv | 10.1093/rheumatology/keab740 |
| format | Article |
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Spondyloarthritis (SpA) comprises a group of chronic inflammatory diseases with overlapping clinical, genetic and pathophysiological features including back pain, peripheral arthritis, psoriasis, enthesitis and dactylitis. Several cytokines are involved in the pathogenesis of SpA, variously contributing to each clinical manifestation. Many SpA-associated cytokines, including IL-23, IL-17, IL-6, type I/II interferon and tumour necrosis factor signal directly or indirectly via the Janus kinase (JAK)–signal transducer and activator of transcription pathway. JAK signalling also regulates development and maturation of cells of the innate and adaptive immune systems. Accordingly, disruption of this signalling pathway by small molecule oral JAK inhibitors can inhibit signalling implicated in SpA pathogenesis. Herein we discuss the role of JAK signalling in the pathogenesis of SpA and summarize the safety and efficacy of JAK inhibition by reference to relevant SpA clinical trials.</description><identifier>ISSN: 1462-0324</identifier><identifier>EISSN: 1462-0332</identifier><identifier>DOI: 10.1093/rheumatology/keab740</identifier><identifier>PMID: 34668515</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Cytokines - metabolism ; Humans ; Janus Kinase Inhibitors - pharmacology ; Janus Kinase Inhibitors - therapeutic use ; Janus Kinases ; Review ; Signal Transduction ; Spondylarthritis - drug therapy ; STAT Transcription Factors - metabolism</subject><ispartof>Rheumatology (Oxford, England), 2022-05, Vol.61 (5), p.1783-1794</ispartof><rights>The Author(s) 2021. Published by Oxford University Press on behalf of the British Society for Rheumatology. 2021</rights><rights>The Author(s) 2021. Published by Oxford University Press on behalf of the British Society for Rheumatology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-148a3e8dd91aeaee2aec1e34ba2b6b8e3a7cbca15f3bf07f1be2cad730a34d7b3</citedby><cites>FETCH-LOGICAL-c448t-148a3e8dd91aeaee2aec1e34ba2b6b8e3a7cbca15f3bf07f1be2cad730a34d7b3</cites><orcidid>0000-0002-7794-6844 ; 0000-0002-2709-6685 ; 0000-0002-1291-1755</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,1584,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34668515$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McInnes, Iain B</creatorcontrib><creatorcontrib>Szekanecz, Zoltán</creatorcontrib><creatorcontrib>McGonagle, Dennis</creatorcontrib><creatorcontrib>Maksymowych, Walter P</creatorcontrib><creatorcontrib>Pfeil, Alexander</creatorcontrib><creatorcontrib>Lippe, Ralph</creatorcontrib><creatorcontrib>Song, In-Ho</creatorcontrib><creatorcontrib>Lertratanakul, Apinya</creatorcontrib><creatorcontrib>Sornasse, Thierry</creatorcontrib><creatorcontrib>Biljan, Ana</creatorcontrib><creatorcontrib>Deodhar, Atul</creatorcontrib><title>A review of JAK–STAT signalling in the pathogenesis of spondyloarthritis and the role of JAK inhibition</title><title>Rheumatology (Oxford, England)</title><addtitle>Rheumatology (Oxford)</addtitle><description>Abstract
Spondyloarthritis (SpA) comprises a group of chronic inflammatory diseases with overlapping clinical, genetic and pathophysiological features including back pain, peripheral arthritis, psoriasis, enthesitis and dactylitis. Several cytokines are involved in the pathogenesis of SpA, variously contributing to each clinical manifestation. Many SpA-associated cytokines, including IL-23, IL-17, IL-6, type I/II interferon and tumour necrosis factor signal directly or indirectly via the Janus kinase (JAK)–signal transducer and activator of transcription pathway. JAK signalling also regulates development and maturation of cells of the innate and adaptive immune systems. Accordingly, disruption of this signalling pathway by small molecule oral JAK inhibitors can inhibit signalling implicated in SpA pathogenesis. Herein we discuss the role of JAK signalling in the pathogenesis of SpA and summarize the safety and efficacy of JAK inhibition by reference to relevant SpA clinical trials.</description><subject>Cytokines - metabolism</subject><subject>Humans</subject><subject>Janus Kinase Inhibitors - pharmacology</subject><subject>Janus Kinase Inhibitors - therapeutic use</subject><subject>Janus Kinases</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Spondylarthritis - drug therapy</subject><subject>STAT Transcription Factors - metabolism</subject><issn>1462-0324</issn><issn>1462-0332</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>TOX</sourceid><sourceid>EIF</sourceid><recordid>eNqNkctu2zAQRYkiQe26_YOi0DIb16RIPbwpYBhN8zCQRdw1MZRGEluaVEgphXf5h_5hviRK7BjOLisSnHPPELiEfGX0O6NzPvMN9hvonHH1dvYXQWWCfiBjJtJ4SjmPTw73WIzIpxD-UEoTxvOPZMRFmuYJS8ZELyKP9xr_Ra6KrhbXjw__b9eLdRR0bcEYbetI26hrMGqha1yNFoMOz3BonS23xoHvGq-74RFs-UJ6Z3CvG8KNVsPU2c_ktAIT8Mv-nJDf5z_Xy4vp6ubX5XKxmhZC5N2UiRw45mU5Z4CAGAMWDLlQEKtU5cghK1QBLKm4qmhWMYVxAWXGKXBRZopPyI-dt-3VBssCbefByNbrDfitdKDl24nVjazdvZzTjCU8HgRne4F3dz2GTm50KNAYsOj6IOMkF5SlImcDKnZo4V0IHqvDGkblc0vyuCW5b2mIfTv-4iH0WssAzHaA69v3KZ8AiZmoog</recordid><startdate>20220505</startdate><enddate>20220505</enddate><creator>McInnes, Iain B</creator><creator>Szekanecz, Zoltán</creator><creator>McGonagle, Dennis</creator><creator>Maksymowych, Walter P</creator><creator>Pfeil, Alexander</creator><creator>Lippe, Ralph</creator><creator>Song, In-Ho</creator><creator>Lertratanakul, Apinya</creator><creator>Sornasse, Thierry</creator><creator>Biljan, Ana</creator><creator>Deodhar, Atul</creator><general>Oxford University Press</general><scope>TOX</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7794-6844</orcidid><orcidid>https://orcid.org/0000-0002-2709-6685</orcidid><orcidid>https://orcid.org/0000-0002-1291-1755</orcidid></search><sort><creationdate>20220505</creationdate><title>A review of JAK–STAT signalling in the pathogenesis of spondyloarthritis and the role of JAK inhibition</title><author>McInnes, Iain B ; Szekanecz, Zoltán ; McGonagle, Dennis ; Maksymowych, Walter P ; Pfeil, Alexander ; Lippe, Ralph ; Song, In-Ho ; Lertratanakul, Apinya ; Sornasse, Thierry ; Biljan, Ana ; Deodhar, Atul</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-148a3e8dd91aeaee2aec1e34ba2b6b8e3a7cbca15f3bf07f1be2cad730a34d7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Cytokines - metabolism</topic><topic>Humans</topic><topic>Janus Kinase Inhibitors - pharmacology</topic><topic>Janus Kinase Inhibitors - therapeutic use</topic><topic>Janus Kinases</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Spondylarthritis - drug therapy</topic><topic>STAT Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McInnes, Iain B</creatorcontrib><creatorcontrib>Szekanecz, Zoltán</creatorcontrib><creatorcontrib>McGonagle, Dennis</creatorcontrib><creatorcontrib>Maksymowych, Walter P</creatorcontrib><creatorcontrib>Pfeil, Alexander</creatorcontrib><creatorcontrib>Lippe, Ralph</creatorcontrib><creatorcontrib>Song, In-Ho</creatorcontrib><creatorcontrib>Lertratanakul, Apinya</creatorcontrib><creatorcontrib>Sornasse, Thierry</creatorcontrib><creatorcontrib>Biljan, Ana</creatorcontrib><creatorcontrib>Deodhar, Atul</creatorcontrib><collection>Oxford Journals Open Access</collection><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>Rheumatology (Oxford, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McInnes, Iain B</au><au>Szekanecz, Zoltán</au><au>McGonagle, Dennis</au><au>Maksymowych, Walter P</au><au>Pfeil, Alexander</au><au>Lippe, Ralph</au><au>Song, In-Ho</au><au>Lertratanakul, Apinya</au><au>Sornasse, Thierry</au><au>Biljan, Ana</au><au>Deodhar, Atul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A review of JAK–STAT signalling in the pathogenesis of spondyloarthritis and the role of JAK inhibition</atitle><jtitle>Rheumatology (Oxford, England)</jtitle><addtitle>Rheumatology (Oxford)</addtitle><date>2022-05-05</date><risdate>2022</risdate><volume>61</volume><issue>5</issue><spage>1783</spage><epage>1794</epage><pages>1783-1794</pages><issn>1462-0324</issn><eissn>1462-0332</eissn><abstract>Abstract
Spondyloarthritis (SpA) comprises a group of chronic inflammatory diseases with overlapping clinical, genetic and pathophysiological features including back pain, peripheral arthritis, psoriasis, enthesitis and dactylitis. Several cytokines are involved in the pathogenesis of SpA, variously contributing to each clinical manifestation. Many SpA-associated cytokines, including IL-23, IL-17, IL-6, type I/II interferon and tumour necrosis factor signal directly or indirectly via the Janus kinase (JAK)–signal transducer and activator of transcription pathway. JAK signalling also regulates development and maturation of cells of the innate and adaptive immune systems. Accordingly, disruption of this signalling pathway by small molecule oral JAK inhibitors can inhibit signalling implicated in SpA pathogenesis. Herein we discuss the role of JAK signalling in the pathogenesis of SpA and summarize the safety and efficacy of JAK inhibition by reference to relevant SpA clinical trials.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>34668515</pmid><doi>10.1093/rheumatology/keab740</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-7794-6844</orcidid><orcidid>https://orcid.org/0000-0002-2709-6685</orcidid><orcidid>https://orcid.org/0000-0002-1291-1755</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Cytokines - metabolism Humans Janus Kinase Inhibitors - pharmacology Janus Kinase Inhibitors - therapeutic use Janus Kinases Review Signal Transduction Spondylarthritis - drug therapy STAT Transcription Factors - metabolism |
| title | A review of JAK–STAT signalling in the pathogenesis of spondyloarthritis and the role of JAK inhibition |
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