Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic systemic inflammation causing progressive joint damage that can lead to lifelong disability. The pathogenesis of RA involves a complex network of various cytokines and cells that trigger synovial cell proliferation and cause...
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| Veröffentlicht in: | International journal of molecular sciences 2021-10, Vol.22 (20), p.10922 |
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| description | Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic systemic inflammation causing progressive joint damage that can lead to lifelong disability. The pathogenesis of RA involves a complex network of various cytokines and cells that trigger synovial cell proliferation and cause damage to both cartilage and bone. Involvement of the cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 is central to the pathogenesis of RA, but recent research has revealed that other cytokines such as IL-7, IL-17, IL-21, IL-23, granulocyte macrophage colony-stimulating factor (GM-CSF), IL-1β, IL-18, IL-33, and IL-2 also play a role. Clarification of RA pathology has led to the development of therapeutic agents such as biological disease-modifying anti-rheumatic drugs (DMARDs) and Janus kinase (JAK) inhibitors, and further details of the immunological background to RA are emerging. This review covers existing knowledge regarding the roles of cytokines, related immune cells and the immune system in RA, manipulation of which may offer the potential for even safer and more effective treatments in the future. |
| doi_str_mv | 10.3390/ijms222010922 |
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The pathogenesis of RA involves a complex network of various cytokines and cells that trigger synovial cell proliferation and cause damage to both cartilage and bone. Involvement of the cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 is central to the pathogenesis of RA, but recent research has revealed that other cytokines such as IL-7, IL-17, IL-21, IL-23, granulocyte macrophage colony-stimulating factor (GM-CSF), IL-1β, IL-18, IL-33, and IL-2 also play a role. Clarification of RA pathology has led to the development of therapeutic agents such as biological disease-modifying anti-rheumatic drugs (DMARDs) and Janus kinase (JAK) inhibitors, and further details of the immunological background to RA are emerging. This review covers existing knowledge regarding the roles of cytokines, related immune cells and the immune system in RA, manipulation of which may offer the potential for even safer and more effective treatments in the future.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms222010922</identifier><identifier>PMID: 34681582</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Antirheumatic Agents - therapeutic use ; Arthritis ; Arthritis, Rheumatoid - drug therapy ; Arthritis, Rheumatoid - metabolism ; Arthritis, Rheumatoid - pathology ; Autoimmune diseases ; Bone tumors ; Cartilage ; Cell proliferation ; Chemical compounds ; Colony-stimulating factor ; Cytokines ; Cytokines - metabolism ; DNA methylation ; Drug development ; Epigenesis, Genetic ; Fibroblasts ; Gene expression ; Granulocyte-macrophage colony-stimulating factor ; Granulocyte-Macrophage Colony-Stimulating Factor - metabolism ; Humans ; IL-1β ; Immune system ; Immunology ; Immunosuppressive agents ; Interleukin 17 ; Interleukin 18 ; Interleukin 2 ; Interleukin 21 ; Interleukin 23 ; Interleukin 7 ; Interleukin-6 - metabolism ; Janus kinase ; Kinases ; Lymphocytes ; Pathogenesis ; Pharmacology ; Protein Kinase Inhibitors - therapeutic use ; Receptors, Tumor Necrosis Factor - metabolism ; Review ; Rheumatoid arthritis ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>International journal of molecular sciences, 2021-10, Vol.22 (20), p.10922</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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The pathogenesis of RA involves a complex network of various cytokines and cells that trigger synovial cell proliferation and cause damage to both cartilage and bone. Involvement of the cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 is central to the pathogenesis of RA, but recent research has revealed that other cytokines such as IL-7, IL-17, IL-21, IL-23, granulocyte macrophage colony-stimulating factor (GM-CSF), IL-1β, IL-18, IL-33, and IL-2 also play a role. Clarification of RA pathology has led to the development of therapeutic agents such as biological disease-modifying anti-rheumatic drugs (DMARDs) and Janus kinase (JAK) inhibitors, and further details of the immunological background to RA are emerging. This review covers existing knowledge regarding the roles of cytokines, related immune cells and the immune system in RA, manipulation of which may offer the potential for even safer and more effective treatments in the future.</description><subject>Antirheumatic Agents - therapeutic use</subject><subject>Arthritis</subject><subject>Arthritis, Rheumatoid - drug therapy</subject><subject>Arthritis, Rheumatoid - metabolism</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Autoimmune diseases</subject><subject>Bone tumors</subject><subject>Cartilage</subject><subject>Cell proliferation</subject><subject>Chemical compounds</subject><subject>Colony-stimulating factor</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>DNA methylation</subject><subject>Drug development</subject><subject>Epigenesis, Genetic</subject><subject>Fibroblasts</subject><subject>Gene expression</subject><subject>Granulocyte-macrophage colony-stimulating factor</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - metabolism</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Immunosuppressive agents</subject><subject>Interleukin 17</subject><subject>Interleukin 18</subject><subject>Interleukin 2</subject><subject>Interleukin 21</subject><subject>Interleukin 23</subject><subject>Interleukin 7</subject><subject>Interleukin-6 - metabolism</subject><subject>Janus kinase</subject><subject>Kinases</subject><subject>Lymphocytes</subject><subject>Pathogenesis</subject><subject>Pharmacology</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Receptors, Tumor Necrosis Factor - metabolism</subject><subject>Review</subject><subject>Rheumatoid arthritis</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1LxDAQxYMofqwevUrBi5dqMkna5KCwLH6BqIieQ9qm26zbRpNU8b-3uqusXmYG5sdj3jyE9gk-plTiEztrAwBggiXAGtomDCDFOMvXV-YttBPCDGOgwOUm2qIsE4QL2Eank4_onm1nklsT351_DontktiY5F7Hxk1NZ4INiauTh8b0rY7OVsnYx8bbaMMu2qj1PJi9ZR-hp4vzx8lVenN3eT0Z36QlEySmAkvCc1JxLTmmZVFCJYWmvOYmw6zIgbMq41AyluGK1gJq4NQQk3MsC1loOkJnC92XvmhNVZouej1XL9622n8op636u-lso6buTQlOZQ50EDhaCnj32psQVWtDaeZz3RnXBwVcsFwOn5IDevgPnbned4O9b4pRTIYyQumCKr0LwZv69xiC1Vcw6k8wA3-w6uCX_kmCfgKrcYjE</recordid><startdate>20211010</startdate><enddate>20211010</enddate><creator>Kondo, Naoki</creator><creator>Kuroda, Takeshi</creator><creator>Kobayashi, Daisuke</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8985-3055</orcidid><orcidid>https://orcid.org/0000-0002-0384-8678</orcidid></search><sort><creationdate>20211010</creationdate><title>Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis</title><author>Kondo, Naoki ; 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The pathogenesis of RA involves a complex network of various cytokines and cells that trigger synovial cell proliferation and cause damage to both cartilage and bone. Involvement of the cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 is central to the pathogenesis of RA, but recent research has revealed that other cytokines such as IL-7, IL-17, IL-21, IL-23, granulocyte macrophage colony-stimulating factor (GM-CSF), IL-1β, IL-18, IL-33, and IL-2 also play a role. Clarification of RA pathology has led to the development of therapeutic agents such as biological disease-modifying anti-rheumatic drugs (DMARDs) and Janus kinase (JAK) inhibitors, and further details of the immunological background to RA are emerging. This review covers existing knowledge regarding the roles of cytokines, related immune cells and the immune system in RA, manipulation of which may offer the potential for even safer and more effective treatments in the future.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>34681582</pmid><doi>10.3390/ijms222010922</doi><orcidid>https://orcid.org/0000-0002-8985-3055</orcidid><orcidid>https://orcid.org/0000-0002-0384-8678</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antirheumatic Agents - therapeutic use Arthritis Arthritis, Rheumatoid - drug therapy Arthritis, Rheumatoid - metabolism Arthritis, Rheumatoid - pathology Autoimmune diseases Bone tumors Cartilage Cell proliferation Chemical compounds Colony-stimulating factor Cytokines Cytokines - metabolism DNA methylation Drug development Epigenesis, Genetic Fibroblasts Gene expression Granulocyte-macrophage colony-stimulating factor Granulocyte-Macrophage Colony-Stimulating Factor - metabolism Humans IL-1β Immune system Immunology Immunosuppressive agents Interleukin 17 Interleukin 18 Interleukin 2 Interleukin 21 Interleukin 23 Interleukin 7 Interleukin-6 - metabolism Janus kinase Kinases Lymphocytes Pathogenesis Pharmacology Protein Kinase Inhibitors - therapeutic use Receptors, Tumor Necrosis Factor - metabolism Review Rheumatoid arthritis Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis |
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