The role of interleukin-33 in pathogenesis of bronchial asthma. New experimental data
Interleukin-33 (IL-33) belongs to the IL-1 cytokine family and plays an important role in modulating immune system by inducing Th2 immune response via the ST2 membrane receptor. Epithelial cells are the major producers of IL-33. However, IL-33 is also secreted by other cells, e.g., bone marrow cells...
Gespeichert in:
Veröffentlicht in: | Biochemistry (Moscow) 2018, Vol.83 (1), p.13-25 |
---|---|
Hauptverfasser: | , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 25 |
---|---|
container_issue | 1 |
container_start_page | 13 |
container_title | Biochemistry (Moscow) |
container_volume | 83 |
creator | Khaitov, M. R. Gaisina, A. R. Shilovskiy, I. P. Smirnov, V. V. Ramenskaia, G. V. Nikonova, A. A. Khaitov, R. M. |
description | Interleukin-33 (IL-33) belongs to the IL-1 cytokine family and plays an important role in modulating immune system by inducing Th2 immune response via the ST2 membrane receptor. Epithelial cells are the major producers of IL-33. However, IL-33 is also secreted by other cells, e.g., bone marrow cells, dendritic cells, macrophages, and mast cells. IL-33 targets a broad range of cell types bearing the ST2 surface receptor. Many ST2-positive cells, such as Th2 cells, mast cells, basophils, and eosinophils, are involved in the development of allergic bronchial asthma (BA). This suggests that IL-33 directly participates in BA pathogenesis. Currently, the role of IL-33 in pathogenesis of inflammatory disorders, including BA, has been extensively investigated using clinical samples collected from patients, as well as asthma animal models. In particular, numerous studies on blocking IL-33 and its receptor by monoclonal antibodies in asthma mouse model have been performed over the last several years; IL-33-and ST2-deficient transgenic mice have also been generated. In this review, we summarized and analyzed the data on the role of IL-33 in BA pathogenesis and the prospects for creating new treatments for BA. |
doi_str_mv | 10.1134/S0006297918010029 |
format | Article |
fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2013784611</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A541102954</galeid><sourcerecordid>A541102954</sourcerecordid><originalsourceid>FETCH-LOGICAL-c439t-d9abc16a72c8c9e9ab2693f3b0cab39af2c390c8240f3cd8132cb6b7c61b159e3</originalsourceid><addsrcrecordid>eNp1kU9v1DAQxS1URJeFD8ClitQLlyy2x_HGx6qigFTBgfZsOc5k121ib-1Epd8eR7u0_CnywRq_33sazxDyjtEVYyA-fKeUSq7WitWUUcrVC7JgktYlUEGPyGKWy1k_Jq9TusklpwpekWOuKhBSigW5vtpiEUOPRegK50eMPU63zpcAuSx2ZtyGDXpMLs1EE4O3W2f6wqRxO5hV8RXvC_yxw-gG9GMWWjOaN-RlZ_qEbw_3klxffLw6_1xefvv05fzssrQC1Fi2yjSWSbPmtrYKc8Wlgg4aak0DynTcgqK25oJ2YNuaAbeNbNZWsoZVCmFJ3u9zdzHcTZhGPbhkse-NxzAlzSmDdS1kntaSnP6F3oQp-tydZkqBAFYBfaI2pkftfBfGaOwcqs8qwViecSUytXqGyqfFwdngsXP5_Q8D2xtsDClF7PQuz8vEB82onlep_1ll9pwcGp6aAdtHx6_dZYDvgZQlv8H424_-m_oT6wOlSg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1993431530</pqid></control><display><type>article</type><title>The role of interleukin-33 in pathogenesis of bronchial asthma. New experimental data</title><source>SpringerLink (Online service)</source><creator>Khaitov, M. R. ; Gaisina, A. R. ; Shilovskiy, I. P. ; Smirnov, V. V. ; Ramenskaia, G. V. ; Nikonova, A. A. ; Khaitov, R. M.</creator><creatorcontrib>Khaitov, M. R. ; Gaisina, A. R. ; Shilovskiy, I. P. ; Smirnov, V. V. ; Ramenskaia, G. V. ; Nikonova, A. A. ; Khaitov, R. M.</creatorcontrib><description>Interleukin-33 (IL-33) belongs to the IL-1 cytokine family and plays an important role in modulating immune system by inducing Th2 immune response via the ST2 membrane receptor. Epithelial cells are the major producers of IL-33. However, IL-33 is also secreted by other cells, e.g., bone marrow cells, dendritic cells, macrophages, and mast cells. IL-33 targets a broad range of cell types bearing the ST2 surface receptor. Many ST2-positive cells, such as Th2 cells, mast cells, basophils, and eosinophils, are involved in the development of allergic bronchial asthma (BA). This suggests that IL-33 directly participates in BA pathogenesis. Currently, the role of IL-33 in pathogenesis of inflammatory disorders, including BA, has been extensively investigated using clinical samples collected from patients, as well as asthma animal models. In particular, numerous studies on blocking IL-33 and its receptor by monoclonal antibodies in asthma mouse model have been performed over the last several years; IL-33-and ST2-deficient transgenic mice have also been generated. In this review, we summarized and analyzed the data on the role of IL-33 in BA pathogenesis and the prospects for creating new treatments for BA.</description><identifier>ISSN: 0006-2979</identifier><identifier>EISSN: 1608-3040</identifier><identifier>DOI: 10.1134/S0006297918010029</identifier><identifier>PMID: 29534664</identifier><language>eng</language><publisher>Moscow: Pleiades Publishing</publisher><subject>Animal models ; Asthma ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Bioorganic Chemistry ; Bone marrow ; Cytokines ; Data processing ; Dendritic cells ; Eosinophils ; Epithelial cells ; Health aspects ; Helper cells ; Immune response ; Immune system ; Inflammatory diseases ; Interleukin 1 ; Interleukins ; Leukocytes (basophilic) ; Leukocytes (eosinophilic) ; Life Sciences ; Lymphocytes T ; Macrophages ; Mast cells ; Microbiology ; Monoclonal antibodies ; Pathogenesis ; Physiological aspects ; Review ; Rodents ; Transgenic mice</subject><ispartof>Biochemistry (Moscow), 2018, Vol.83 (1), p.13-25</ispartof><rights>Pleiades Publishing, Ltd. 2018</rights><rights>COPYRIGHT 2018 Springer</rights><rights>Biochemistry (Moscow) is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-d9abc16a72c8c9e9ab2693f3b0cab39af2c390c8240f3cd8132cb6b7c61b159e3</citedby><cites>FETCH-LOGICAL-c439t-d9abc16a72c8c9e9ab2693f3b0cab39af2c390c8240f3cd8132cb6b7c61b159e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1134/S0006297918010029$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1134/S0006297918010029$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29534664$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Khaitov, M. R.</creatorcontrib><creatorcontrib>Gaisina, A. R.</creatorcontrib><creatorcontrib>Shilovskiy, I. P.</creatorcontrib><creatorcontrib>Smirnov, V. V.</creatorcontrib><creatorcontrib>Ramenskaia, G. V.</creatorcontrib><creatorcontrib>Nikonova, A. A.</creatorcontrib><creatorcontrib>Khaitov, R. M.</creatorcontrib><title>The role of interleukin-33 in pathogenesis of bronchial asthma. New experimental data</title><title>Biochemistry (Moscow)</title><addtitle>Biochemistry Moscow</addtitle><addtitle>Biochemistry (Mosc)</addtitle><description>Interleukin-33 (IL-33) belongs to the IL-1 cytokine family and plays an important role in modulating immune system by inducing Th2 immune response via the ST2 membrane receptor. Epithelial cells are the major producers of IL-33. However, IL-33 is also secreted by other cells, e.g., bone marrow cells, dendritic cells, macrophages, and mast cells. IL-33 targets a broad range of cell types bearing the ST2 surface receptor. Many ST2-positive cells, such as Th2 cells, mast cells, basophils, and eosinophils, are involved in the development of allergic bronchial asthma (BA). This suggests that IL-33 directly participates in BA pathogenesis. Currently, the role of IL-33 in pathogenesis of inflammatory disorders, including BA, has been extensively investigated using clinical samples collected from patients, as well as asthma animal models. In particular, numerous studies on blocking IL-33 and its receptor by monoclonal antibodies in asthma mouse model have been performed over the last several years; IL-33-and ST2-deficient transgenic mice have also been generated. In this review, we summarized and analyzed the data on the role of IL-33 in BA pathogenesis and the prospects for creating new treatments for BA.</description><subject>Animal models</subject><subject>Asthma</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bioorganic Chemistry</subject><subject>Bone marrow</subject><subject>Cytokines</subject><subject>Data processing</subject><subject>Dendritic cells</subject><subject>Eosinophils</subject><subject>Epithelial cells</subject><subject>Health aspects</subject><subject>Helper cells</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Inflammatory diseases</subject><subject>Interleukin 1</subject><subject>Interleukins</subject><subject>Leukocytes (basophilic)</subject><subject>Leukocytes (eosinophilic)</subject><subject>Life Sciences</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Mast cells</subject><subject>Microbiology</subject><subject>Monoclonal antibodies</subject><subject>Pathogenesis</subject><subject>Physiological aspects</subject><subject>Review</subject><subject>Rodents</subject><subject>Transgenic mice</subject><issn>0006-2979</issn><issn>1608-3040</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kU9v1DAQxS1URJeFD8ClitQLlyy2x_HGx6qigFTBgfZsOc5k121ib-1Epd8eR7u0_CnywRq_33sazxDyjtEVYyA-fKeUSq7WitWUUcrVC7JgktYlUEGPyGKWy1k_Jq9TusklpwpekWOuKhBSigW5vtpiEUOPRegK50eMPU63zpcAuSx2ZtyGDXpMLs1EE4O3W2f6wqRxO5hV8RXvC_yxw-gG9GMWWjOaN-RlZ_qEbw_3klxffLw6_1xefvv05fzssrQC1Fi2yjSWSbPmtrYKc8Wlgg4aak0DynTcgqK25oJ2YNuaAbeNbNZWsoZVCmFJ3u9zdzHcTZhGPbhkse-NxzAlzSmDdS1kntaSnP6F3oQp-tydZkqBAFYBfaI2pkftfBfGaOwcqs8qwViecSUytXqGyqfFwdngsXP5_Q8D2xtsDClF7PQuz8vEB82onlep_1ll9pwcGp6aAdtHx6_dZYDvgZQlv8H424_-m_oT6wOlSg</recordid><startdate>2018</startdate><enddate>2018</enddate><creator>Khaitov, M. R.</creator><creator>Gaisina, A. R.</creator><creator>Shilovskiy, I. P.</creator><creator>Smirnov, V. V.</creator><creator>Ramenskaia, G. V.</creator><creator>Nikonova, A. A.</creator><creator>Khaitov, R. M.</creator><general>Pleiades Publishing</general><general>Springer</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</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>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>2018</creationdate><title>The role of interleukin-33 in pathogenesis of bronchial asthma. New experimental data</title><author>Khaitov, M. R. ; Gaisina, A. R. ; Shilovskiy, I. P. ; Smirnov, V. V. ; Ramenskaia, G. V. ; Nikonova, A. A. ; Khaitov, R. M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-d9abc16a72c8c9e9ab2693f3b0cab39af2c390c8240f3cd8132cb6b7c61b159e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animal models</topic><topic>Asthma</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bioorganic Chemistry</topic><topic>Bone marrow</topic><topic>Cytokines</topic><topic>Data processing</topic><topic>Dendritic cells</topic><topic>Eosinophils</topic><topic>Epithelial cells</topic><topic>Health aspects</topic><topic>Helper cells</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Inflammatory diseases</topic><topic>Interleukin 1</topic><topic>Interleukins</topic><topic>Leukocytes (basophilic)</topic><topic>Leukocytes (eosinophilic)</topic><topic>Life Sciences</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Mast cells</topic><topic>Microbiology</topic><topic>Monoclonal antibodies</topic><topic>Pathogenesis</topic><topic>Physiological aspects</topic><topic>Review</topic><topic>Rodents</topic><topic>Transgenic mice</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Khaitov, M. R.</creatorcontrib><creatorcontrib>Gaisina, A. R.</creatorcontrib><creatorcontrib>Shilovskiy, I. P.</creatorcontrib><creatorcontrib>Smirnov, V. V.</creatorcontrib><creatorcontrib>Ramenskaia, G. V.</creatorcontrib><creatorcontrib>Nikonova, A. A.</creatorcontrib><creatorcontrib>Khaitov, R. M.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science 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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>ProQuest Biological Science Journals</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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemistry (Moscow)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khaitov, M. R.</au><au>Gaisina, A. R.</au><au>Shilovskiy, I. P.</au><au>Smirnov, V. V.</au><au>Ramenskaia, G. V.</au><au>Nikonova, A. A.</au><au>Khaitov, R. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of interleukin-33 in pathogenesis of bronchial asthma. New experimental data</atitle><jtitle>Biochemistry (Moscow)</jtitle><stitle>Biochemistry Moscow</stitle><addtitle>Biochemistry (Mosc)</addtitle><date>2018</date><risdate>2018</risdate><volume>83</volume><issue>1</issue><spage>13</spage><epage>25</epage><pages>13-25</pages><issn>0006-2979</issn><eissn>1608-3040</eissn><abstract>Interleukin-33 (IL-33) belongs to the IL-1 cytokine family and plays an important role in modulating immune system by inducing Th2 immune response via the ST2 membrane receptor. Epithelial cells are the major producers of IL-33. However, IL-33 is also secreted by other cells, e.g., bone marrow cells, dendritic cells, macrophages, and mast cells. IL-33 targets a broad range of cell types bearing the ST2 surface receptor. Many ST2-positive cells, such as Th2 cells, mast cells, basophils, and eosinophils, are involved in the development of allergic bronchial asthma (BA). This suggests that IL-33 directly participates in BA pathogenesis. Currently, the role of IL-33 in pathogenesis of inflammatory disorders, including BA, has been extensively investigated using clinical samples collected from patients, as well as asthma animal models. In particular, numerous studies on blocking IL-33 and its receptor by monoclonal antibodies in asthma mouse model have been performed over the last several years; IL-33-and ST2-deficient transgenic mice have also been generated. In this review, we summarized and analyzed the data on the role of IL-33 in BA pathogenesis and the prospects for creating new treatments for BA.</abstract><cop>Moscow</cop><pub>Pleiades Publishing</pub><pmid>29534664</pmid><doi>10.1134/S0006297918010029</doi><tpages>13</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0006-2979 |
ispartof | Biochemistry (Moscow), 2018, Vol.83 (1), p.13-25 |
issn | 0006-2979 1608-3040 |
language | eng |
recordid | cdi_proquest_miscellaneous_2013784611 |
source | SpringerLink (Online service) |
subjects | Animal models Asthma Biochemistry Biomedical and Life Sciences Biomedicine Bioorganic Chemistry Bone marrow Cytokines Data processing Dendritic cells Eosinophils Epithelial cells Health aspects Helper cells Immune response Immune system Inflammatory diseases Interleukin 1 Interleukins Leukocytes (basophilic) Leukocytes (eosinophilic) Life Sciences Lymphocytes T Macrophages Mast cells Microbiology Monoclonal antibodies Pathogenesis Physiological aspects Review Rodents Transgenic mice |
title | The role of interleukin-33 in pathogenesis of bronchial asthma. New experimental data |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T10%3A25%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20role%20of%20interleukin-33%20in%20pathogenesis%20of%20bronchial%20asthma.%20New%20experimental%20data&rft.jtitle=Biochemistry%20(Moscow)&rft.au=Khaitov,%20M.%20R.&rft.date=2018&rft.volume=83&rft.issue=1&rft.spage=13&rft.epage=25&rft.pages=13-25&rft.issn=0006-2979&rft.eissn=1608-3040&rft_id=info:doi/10.1134/S0006297918010029&rft_dat=%3Cgale_proqu%3EA541102954%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1993431530&rft_id=info:pmid/29534664&rft_galeid=A541102954&rfr_iscdi=true |