IL-6 in inflammation, immunity, and disease.
Identifieur interne : 002421 ( Main/Exploration ); précédent : 002420; suivant : 002422IL-6 in inflammation, immunity, and disease.
Auteurs : Toshio Tanaka [Japon] ; Masashi Narazaki [Japon] ; Tadamitsu Kishimoto [Japon]Source :
- Cold Spring Harbor perspectives in biology [ 1943-0264 ] ; 2014.
Descripteurs français
- KwdFr :
- Anticorps monoclonaux humanisés (usage thérapeutique), Humains, Inflammation (immunologie), Interleukine-6 (immunologie), Interleukine-6 (métabolisme), Interleukine-6 (physiologie), Modèles immunologiques, Récepteurs à hydrocarbure aromatique (immunologie), Récepteurs à hydrocarbure aromatique (métabolisme), Récepteurs à hydrocarbure aromatique (physiologie), Régulation de l'expression des gènes, Transduction du signal.
- MESH :
- immunologie : Inflammation, Interleukine-6, Récepteurs à hydrocarbure aromatique.
- métabolisme : Interleukine-6, Récepteurs à hydrocarbure aromatique.
- physiologie : Interleukine-6, Récepteurs à hydrocarbure aromatique.
- usage thérapeutique : Anticorps monoclonaux humanisés.
- Humains, Modèles immunologiques, Régulation de l'expression des gènes, Transduction du signal.
English descriptors
- KwdEn :
- Antibodies, Monoclonal, Humanized (therapeutic use), Gene Expression Regulation, Humans, Inflammation (immunology), Interleukin-6 (immunology), Interleukin-6 (metabolism), Interleukin-6 (physiology), Models, Immunological, Receptors, Aryl Hydrocarbon (immunology), Receptors, Aryl Hydrocarbon (metabolism), Receptors, Aryl Hydrocarbon (physiology), Signal Transduction.
- MESH :
- chemical , immunology : Interleukin-6, Receptors, Aryl Hydrocarbon.
- chemical , metabolism : Interleukin-6, Receptors, Aryl Hydrocarbon.
- chemical , physiology : Interleukin-6, Receptors, Aryl Hydrocarbon.
- chemical , therapeutic use : Antibodies, Monoclonal, Humanized.
- immunology : Inflammation.
- Gene Expression Regulation, Humans, Models, Immunological, Signal Transduction.
Abstract
Interleukin 6 (IL-6), promptly and transiently produced in response to infections and tissue injuries, contributes to host defense through the stimulation of acute phase responses, hematopoiesis, and immune reactions. Although its expression is strictly controlled by transcriptional and posttranscriptional mechanisms, dysregulated continual synthesis of IL-6 plays a pathological effect on chronic inflammation and autoimmunity. For this reason, tocilizumab, a humanized anti-IL-6 receptor antibody was developed. Various clinical trials have since shown the exceptional efficacy of tocilizumab, which resulted in its approval for the treatment of rheumatoid arthritis and juvenile idiopathic arthritis. Moreover, tocilizumab is expected to be effective for other intractable immune-mediated diseases. In this context, the mechanism for the continual synthesis of IL-6 needs to be elucidated to facilitate the development of more specific therapeutic approaches and analysis of the pathogenesis of specific diseases.
DOI: 10.1101/cshperspect.a016295
PubMed: 25190079
Affiliations:
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Le document en format XML
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565-0871</wicri:noRegion></affiliation></author><author><name sortKey="Narazaki, Masashi" sort="Narazaki, Masashi" uniqKey="Narazaki M" first="Masashi" last="Narazaki">Masashi Narazaki</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka University, Osaka 565-0871</wicri:regionArea><wicri:noRegion>Osaka 565-0871</wicri:noRegion></affiliation></author><author><name sortKey="Kishimoto, Tadamitsu" sort="Kishimoto, Tadamitsu" uniqKey="Kishimoto T" first="Tadamitsu" last="Kishimoto">Tadamitsu Kishimoto</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Immune Regulation, World Premier International Immunology Frontier Research Center, 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University Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan Department of Immunopathology, World Premier International Immunology Frontier Research Center, Osaka University, Osaka 565-0871</wicri:regionArea><wicri:noRegion>Osaka 565-0871</wicri:noRegion></affiliation></author><author><name sortKey="Narazaki, Masashi" sort="Narazaki, Masashi" uniqKey="Narazaki M" first="Masashi" last="Narazaki">Masashi Narazaki</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka University, Osaka 565-0871</wicri:regionArea><wicri:noRegion>Osaka 565-0871</wicri:noRegion></affiliation></author><author><name sortKey="Kishimoto, Tadamitsu" sort="Kishimoto, Tadamitsu" uniqKey="Kishimoto T" first="Tadamitsu" last="Kishimoto">Tadamitsu Kishimoto</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Immune Regulation, World Premier International Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Immune Regulation, World Premier International Immunology Frontier Research Center, Osaka University, Osaka 565-0871</wicri:regionArea><wicri:noRegion>Osaka 565-0871</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cold Spring Harbor perspectives in biology</title><idno type="eISSN">1943-0264</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antibodies, Monoclonal, Humanized (therapeutic use)</term><term>Gene Expression 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hematopoiesis, and immune reactions. Although its expression is strictly controlled by transcriptional and posttranscriptional mechanisms, dysregulated continual synthesis of IL-6 plays a pathological effect on chronic inflammation and autoimmunity. For this reason, tocilizumab, a humanized anti-IL-6 receptor antibody was developed. Various clinical trials have since shown the exceptional efficacy of tocilizumab, which resulted in its approval for the treatment of rheumatoid arthritis and juvenile idiopathic arthritis. Moreover, tocilizumab is expected to be effective for other intractable immune-mediated diseases. In this context, the mechanism for the continual synthesis of IL-6 needs to be elucidated to facilitate the development of more specific therapeutic approaches and analysis of the pathogenesis of specific diseases. </div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Tanaka, Toshio" sort="Tanaka, Toshio" uniqKey="Tanaka T" first="Toshio" last="Tanaka">Toshio Tanaka</name></noRegion><name sortKey="Kishimoto, Tadamitsu" sort="Kishimoto, Tadamitsu" uniqKey="Kishimoto T" first="Tadamitsu" last="Kishimoto">Tadamitsu Kishimoto</name><name sortKey="Narazaki, Masashi" sort="Narazaki, Masashi" uniqKey="Narazaki M" first="Masashi" last="Narazaki">Masashi Narazaki</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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