Immunotherapeutic implications of IL-6 blockade for cytokine storm
IL-6 contributes to host defense against infections and tissue injuries. However, exaggerated, excessive synthesis of IL-6 while fighting environmental stress leads to an acute severe systemic inflammatory response known as 'cytokine storm', since high levels of IL-6 can activate the coagu...
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| Veröffentlicht in: | Immunotherapy 2016-07, Vol.8 (8), p.959-970 |
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| container_title | Immunotherapy |
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| creator | Tanaka, Toshio Narazaki, Masashi Kishimoto, Tadamitsu |
| description | IL-6 contributes to host defense against infections and tissue injuries. However, exaggerated, excessive synthesis of IL-6 while fighting environmental stress leads to an acute severe systemic inflammatory response known as 'cytokine storm', since high levels of IL-6 can activate the coagulation pathway and vascular endothelial cells but inhibit myocardial function. Remarkable beneficial effects of IL-6 blockade therapy using a humanized anti-IL-6 receptor antibody, tocilizumab were recently observed in patients with cytokine release syndrome complicated by T-cell engaged therapy. In this review we propose the possibility that IL-6 blockade may constitute a novel therapeutic strategy for other types of cytokine storm, such as the systemic inflammatory response syndrome including sepsis, macrophage activation syndrome and hemophagocytic lymphohistiocytosis. |
| doi_str_mv | 10.2217/imt-2016-0020 |
| format | Article |
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However, exaggerated, excessive synthesis of IL-6 while fighting environmental stress leads to an acute severe systemic inflammatory response known as 'cytokine storm', since high levels of IL-6 can activate the coagulation pathway and vascular endothelial cells but inhibit myocardial function. Remarkable beneficial effects of IL-6 blockade therapy using a humanized anti-IL-6 receptor antibody, tocilizumab were recently observed in patients with cytokine release syndrome complicated by T-cell engaged therapy. 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However, exaggerated, excessive synthesis of IL-6 while fighting environmental stress leads to an acute severe systemic inflammatory response known as 'cytokine storm', since high levels of IL-6 can activate the coagulation pathway and vascular endothelial cells but inhibit myocardial function. Remarkable beneficial effects of IL-6 blockade therapy using a humanized anti-IL-6 receptor antibody, tocilizumab were recently observed in patients with cytokine release syndrome complicated by T-cell engaged therapy. In this review we propose the possibility that IL-6 blockade may constitute a novel therapeutic strategy for other types of cytokine storm, such as the systemic inflammatory response syndrome including sepsis, macrophage activation syndrome and hemophagocytic lymphohistiocytosis.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Antibodies, Monoclonal, Humanized - therapeutic use</subject><subject>Binding sites</subject><subject>Blood Coagulation</subject><subject>Cell activation</subject><subject>Chronic illnesses</subject><subject>Clinical trials</subject><subject>Cytokine storm</subject><subject>Cytokines</subject><subject>Endothelial cells</subject><subject>Endothelium, Vascular - pathology</subject><subject>Environmental stress</subject><subject>Histiocytosis</subject><subject>Humans</subject><subject>IL-6</subject><subject>Immunosuppressive agents</subject><subject>Immunotherapy - methods</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Interleukin 6</subject><subject>Interleukin 6 receptors</subject><subject>Interleukin-6 - immunology</subject><subject>Lymphocytes T</subject><subject>Lymphocytosis</subject><subject>Lymphohistiocytosis, Hemophagocytic - immunology</subject><subject>Lymphohistiocytosis, Hemophagocytic - therapy</subject><subject>Macrophage Activation Syndrome - immunology</subject><subject>Macrophage Activation Syndrome - therapy</subject><subject>Macrophages</subject><subject>Mortality</subject><subject>Patients</subject><subject>Pneumonia</subject><subject>Proteins</subject><subject>Rheumatoid arthritis</subject><subject>Sepsis</subject><subject>Sepsis - immunology</subject><subject>Sepsis - therapy</subject><subject>Signal transduction</subject><subject>Systemic inflammatory response syndrome</subject><subject>tocilizumab</subject><subject>Trauma</subject><issn>1750-743X</issn><issn>1750-7448</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</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>eNp1kD1PwzAQhi0EoqUwsqJILCwBf8VORqj4qFSJBSQ2K3Zs4TaJg-0M_fe4CnRAYro76blXdw8AlwjeYoz4ne1ijiFiOYQYHoE54gXMOaXl8aEnHzNwFsIGQkY5o6dghjkpESv5HDysum7sXfzUvh70GK3KbDe0VtXRuj5kzmSrdc4y2Tq1rRudGecztYtua3udheh8dw5OTN0GffFTF-D96fFt-ZKvX59Xy_t1rgpEY04ll5IZg0vIuVSYVLWCVV00UhPTUFrpEnNpNMNFYQxCFSxK2RSMEAxlIw1ZgJspd_Dua9Qhis4Gpdu27rUbg0AlLFn6j1UJvf6Dbtzo-3SdwAQTmkDIE5VPlPIuBK-NGLztar8TCIq9XJHkir1csZeb-Kuf1FF2ujnQvzYTUE2AGePodVBW90qLaUobViVp_4R_AyHaiC8</recordid><startdate>20160701</startdate><enddate>20160701</enddate><creator>Tanaka, Toshio</creator><creator>Narazaki, Masashi</creator><creator>Kishimoto, Tadamitsu</creator><general>Future Medicine Ltd</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>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>CCPQU</scope><scope>DWQXO</scope><scope>EHMNL</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20160701</creationdate><title>Immunotherapeutic implications of IL-6 blockade for cytokine storm</title><author>Tanaka, Toshio ; Narazaki, Masashi ; Kishimoto, Tadamitsu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-4b7bb6ff28077bc239ac09a5dbe3fd449e827bfe6255ff119058bd563320bdbf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Antibodies, Monoclonal, Humanized - therapeutic use</topic><topic>Binding sites</topic><topic>Blood Coagulation</topic><topic>Cell activation</topic><topic>Chronic illnesses</topic><topic>Clinical trials</topic><topic>Cytokine storm</topic><topic>Cytokines</topic><topic>Endothelial cells</topic><topic>Endothelium, Vascular - pathology</topic><topic>Environmental stress</topic><topic>Histiocytosis</topic><topic>Humans</topic><topic>IL-6</topic><topic>Immunosuppressive agents</topic><topic>Immunotherapy - methods</topic><topic>Inflammation</topic><topic>Inflammatory diseases</topic><topic>Interleukin 6</topic><topic>Interleukin 6 receptors</topic><topic>Interleukin-6 - immunology</topic><topic>Lymphocytes T</topic><topic>Lymphocytosis</topic><topic>Lymphohistiocytosis, Hemophagocytic - immunology</topic><topic>Lymphohistiocytosis, Hemophagocytic - therapy</topic><topic>Macrophage Activation Syndrome - immunology</topic><topic>Macrophage Activation Syndrome - therapy</topic><topic>Macrophages</topic><topic>Mortality</topic><topic>Patients</topic><topic>Pneumonia</topic><topic>Proteins</topic><topic>Rheumatoid arthritis</topic><topic>Sepsis</topic><topic>Sepsis - immunology</topic><topic>Sepsis - therapy</topic><topic>Signal transduction</topic><topic>Systemic inflammatory response syndrome</topic><topic>tocilizumab</topic><topic>Trauma</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tanaka, Toshio</creatorcontrib><creatorcontrib>Narazaki, Masashi</creatorcontrib><creatorcontrib>Kishimoto, Tadamitsu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>UK & Ireland Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Immunotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tanaka, Toshio</au><au>Narazaki, Masashi</au><au>Kishimoto, Tadamitsu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunotherapeutic implications of IL-6 blockade for cytokine storm</atitle><jtitle>Immunotherapy</jtitle><addtitle>Immunotherapy</addtitle><date>2016-07-01</date><risdate>2016</risdate><volume>8</volume><issue>8</issue><spage>959</spage><epage>970</epage><pages>959-970</pages><issn>1750-743X</issn><eissn>1750-7448</eissn><abstract>IL-6 contributes to host defense against infections and tissue injuries. 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| subjects | Animals Anti-Inflammatory Agents - therapeutic use Antibodies, Monoclonal, Humanized - therapeutic use Binding sites Blood Coagulation Cell activation Chronic illnesses Clinical trials Cytokine storm Cytokines Endothelial cells Endothelium, Vascular - pathology Environmental stress Histiocytosis Humans IL-6 Immunosuppressive agents Immunotherapy - methods Inflammation Inflammatory diseases Interleukin 6 Interleukin 6 receptors Interleukin-6 - immunology Lymphocytes T Lymphocytosis Lymphohistiocytosis, Hemophagocytic - immunology Lymphohistiocytosis, Hemophagocytic - therapy Macrophage Activation Syndrome - immunology Macrophage Activation Syndrome - therapy Macrophages Mortality Patients Pneumonia Proteins Rheumatoid arthritis Sepsis Sepsis - immunology Sepsis - therapy Signal transduction Systemic inflammatory response syndrome tocilizumab Trauma |
| title | Immunotherapeutic implications of IL-6 blockade for cytokine storm |
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