Inhibition of IL-17A in atherosclerosis
Abstract Objective To determine the effects of interleukin (IL)-17A inhibition on experimental atherosclerosis. Methods and results ApoE−/− mice were treated with either rat anti-mouse IL-17A, mouse anti-mouse IL-17A or isotype-matched control antibodies for 12 weeks ( n = 8–10 per group). Ldlr−/− m...
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| Veröffentlicht in: | Atherosclerosis 2011-04, Vol.215 (2), p.471-474 |
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| creator | Cheng, Xiang Taleb, Soraya Wang, Jun Tang, Ting-Ting Chen, Jian Gao, Xing-Li Yao, Rui Xie, Jiang-Jiao Yu, Xian Xia, Ni Yan, Xin-Xin Nie, Shao-Fang Liao, Meng-Yang Cheng, Yan Mallat, Ziad Liao, Yu-Hua |
| description | Abstract Objective To determine the effects of interleukin (IL)-17A inhibition on experimental atherosclerosis. Methods and results ApoE−/− mice were treated with either rat anti-mouse IL-17A, mouse anti-mouse IL-17A or isotype-matched control antibodies for 12 weeks ( n = 8–10 per group). Ldlr−/− mice were transplanted with IL-17A-deficient or wild type bone marrow ( n = 8 per group). Rat anti-mouse IL-17A treatment obviously reduced plaque size by 43% ( p < 0.01) without evidence of reduced IL-17A signaling. In contrast, mouse anti-mouse IL-17A treatment and IL-17A deficiency in bone marrow cells did not alter lesion size despite significant reduction of IL-17A production. Conclusions Inhibition of IL-17A signaling does not alter lesion development in Th1-biased C57BL/6 ApoE−/− and Ldlr−/− mice with already low levels of IL-17A production. Alteration of lesion development after repeated injections of rat anti-mouse IL-17A antibody in ApoE−/− mice could not be attributed to blockade of IL-17A signaling. |
| doi_str_mv | 10.1016/j.atherosclerosis.2010.12.034 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_859759622</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>1_s2_0_S0021915011000530</els_id><sourcerecordid>859759622</sourcerecordid><originalsourceid>FETCH-LOGICAL-c497t-8f5beac2e186b616b7acd0bcdcb0dc1b1cd1c1aa0e0396185d9db8c8cca237d3</originalsourceid><addsrcrecordid>eNqNksFO3DAQhq2qVdnSvgLdC-KU7YwdJ86BSgi1sNJKHICzZY8d8DabgJ2txNvjaBcOe-JiH_zNzO_PZuwUYYGA1a_1woyPPg6JumkNacFhOuMLEOUnNkNVNwWWqvzMZgAciwYlHLFvKa0BoKxRfWVHHAWAkDhjZ8v-MdgwhqGfD-18uSqwvpiHfn4w5Tv70pou-R_7_Zjd_f1zd3ldrG6ulpcXq4LKph4L1UrrDXGPqrIVVrY25MCSIwuO0CI5JDQGPIimQiVd46wiRWS4qJ04Zme7tk9xeN76NOpNSOS7zvR-2CatZFPLpuI8k-c7knK-FH2rn2LYmPiiEfRkSq_1wR30ZEoj19lUrj_ZT9rajXfv1W9qMnC6B0wi07XR9JR7vHNllsmlyNzPHdeaQZuHmJn72zxJTroVlE0mrnaEz-L-Bx91ouB78i5ET6N2Q_hw6N8HnagLfcjx_vkXn9bDNvb5dTTqlAv07fQBpvdHzGGkAPEKyo-t_w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>859759622</pqid></control><display><type>article</type><title>Inhibition of IL-17A in atherosclerosis</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Cheng, Xiang ; Taleb, Soraya ; Wang, Jun ; Tang, Ting-Ting ; Chen, Jian ; Gao, Xing-Li ; Yao, Rui ; Xie, Jiang-Jiao ; Yu, Xian ; Xia, Ni ; Yan, Xin-Xin ; Nie, Shao-Fang ; Liao, Meng-Yang ; Cheng, Yan ; Mallat, Ziad ; Liao, Yu-Hua</creator><creatorcontrib>Cheng, Xiang ; Taleb, Soraya ; Wang, Jun ; Tang, Ting-Ting ; Chen, Jian ; Gao, Xing-Li ; Yao, Rui ; Xie, Jiang-Jiao ; Yu, Xian ; Xia, Ni ; Yan, Xin-Xin ; Nie, Shao-Fang ; Liao, Meng-Yang ; Cheng, Yan ; Mallat, Ziad ; Liao, Yu-Hua</creatorcontrib><description>Abstract Objective To determine the effects of interleukin (IL)-17A inhibition on experimental atherosclerosis. Methods and results ApoE−/− mice were treated with either rat anti-mouse IL-17A, mouse anti-mouse IL-17A or isotype-matched control antibodies for 12 weeks ( n = 8–10 per group). Ldlr−/− mice were transplanted with IL-17A-deficient or wild type bone marrow ( n = 8 per group). Rat anti-mouse IL-17A treatment obviously reduced plaque size by 43% ( p < 0.01) without evidence of reduced IL-17A signaling. In contrast, mouse anti-mouse IL-17A treatment and IL-17A deficiency in bone marrow cells did not alter lesion size despite significant reduction of IL-17A production. Conclusions Inhibition of IL-17A signaling does not alter lesion development in Th1-biased C57BL/6 ApoE−/− and Ldlr−/− mice with already low levels of IL-17A production. Alteration of lesion development after repeated injections of rat anti-mouse IL-17A antibody in ApoE−/− mice could not be attributed to blockade of IL-17A signaling.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2010.12.034</identifier><identifier>PMID: 21300351</identifier><language>eng</language><publisher>Amsterdam: Elsevier Ireland Ltd</publisher><subject>Animals ; antibodies ; Antibodies - pharmacology ; Antibody ; Apolipoproteins E - deficiency ; Associated diseases and complications ; Atherosclerosis ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - immunology ; Atherosclerosis - prevention & control ; Biological and medical sciences ; Blood and lymphatic vessels ; bone marrow ; bone marrow cells ; Bone marrow transplantation ; Cardiology. Vascular system ; Cardiovascular ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Female ; IL-17A ; Inflammation ; Interleukin-17 - antagonists & inhibitors ; Interleukin-17 - immunology ; Interleukin-17 - physiology ; interleukins ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Plaque, Atherosclerotic - prevention & control ; Rats ; Receptors, LDL - deficiency ; Signal Transduction - drug effects</subject><ispartof>Atherosclerosis, 2011-04, Vol.215 (2), p.471-474</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2011 Elsevier Ireland Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-8f5beac2e186b616b7acd0bcdcb0dc1b1cd1c1aa0e0396185d9db8c8cca237d3</citedby><cites>FETCH-LOGICAL-c497t-8f5beac2e186b616b7acd0bcdcb0dc1b1cd1c1aa0e0396185d9db8c8cca237d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0021915011000530$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24047253$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21300351$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheng, Xiang</creatorcontrib><creatorcontrib>Taleb, Soraya</creatorcontrib><creatorcontrib>Wang, Jun</creatorcontrib><creatorcontrib>Tang, Ting-Ting</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>Gao, Xing-Li</creatorcontrib><creatorcontrib>Yao, Rui</creatorcontrib><creatorcontrib>Xie, Jiang-Jiao</creatorcontrib><creatorcontrib>Yu, Xian</creatorcontrib><creatorcontrib>Xia, Ni</creatorcontrib><creatorcontrib>Yan, Xin-Xin</creatorcontrib><creatorcontrib>Nie, Shao-Fang</creatorcontrib><creatorcontrib>Liao, Meng-Yang</creatorcontrib><creatorcontrib>Cheng, Yan</creatorcontrib><creatorcontrib>Mallat, Ziad</creatorcontrib><creatorcontrib>Liao, Yu-Hua</creatorcontrib><title>Inhibition of IL-17A in atherosclerosis</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Abstract Objective To determine the effects of interleukin (IL)-17A inhibition on experimental atherosclerosis. Methods and results ApoE−/− mice were treated with either rat anti-mouse IL-17A, mouse anti-mouse IL-17A or isotype-matched control antibodies for 12 weeks ( n = 8–10 per group). Ldlr−/− mice were transplanted with IL-17A-deficient or wild type bone marrow ( n = 8 per group). Rat anti-mouse IL-17A treatment obviously reduced plaque size by 43% ( p < 0.01) without evidence of reduced IL-17A signaling. In contrast, mouse anti-mouse IL-17A treatment and IL-17A deficiency in bone marrow cells did not alter lesion size despite significant reduction of IL-17A production. Conclusions Inhibition of IL-17A signaling does not alter lesion development in Th1-biased C57BL/6 ApoE−/− and Ldlr−/− mice with already low levels of IL-17A production. Alteration of lesion development after repeated injections of rat anti-mouse IL-17A antibody in ApoE−/− mice could not be attributed to blockade of IL-17A signaling.</description><subject>Animals</subject><subject>antibodies</subject><subject>Antibodies - pharmacology</subject><subject>Antibody</subject><subject>Apolipoproteins E - deficiency</subject><subject>Associated diseases and complications</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Atherosclerosis - immunology</subject><subject>Atherosclerosis - prevention & control</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>bone marrow</subject><subject>bone marrow cells</subject><subject>Bone marrow transplantation</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>IL-17A</subject><subject>Inflammation</subject><subject>Interleukin-17 - antagonists & inhibitors</subject><subject>Interleukin-17 - immunology</subject><subject>Interleukin-17 - physiology</subject><subject>interleukins</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Plaque, Atherosclerotic - prevention & control</subject><subject>Rats</subject><subject>Receptors, LDL - deficiency</subject><subject>Signal Transduction - drug effects</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNksFO3DAQhq2qVdnSvgLdC-KU7YwdJ86BSgi1sNJKHICzZY8d8DabgJ2txNvjaBcOe-JiH_zNzO_PZuwUYYGA1a_1woyPPg6JumkNacFhOuMLEOUnNkNVNwWWqvzMZgAciwYlHLFvKa0BoKxRfWVHHAWAkDhjZ8v-MdgwhqGfD-18uSqwvpiHfn4w5Tv70pou-R_7_Zjd_f1zd3ldrG6ulpcXq4LKph4L1UrrDXGPqrIVVrY25MCSIwuO0CI5JDQGPIimQiVd46wiRWS4qJ04Zme7tk9xeN76NOpNSOS7zvR-2CatZFPLpuI8k-c7knK-FH2rn2LYmPiiEfRkSq_1wR30ZEoj19lUrj_ZT9rajXfv1W9qMnC6B0wi07XR9JR7vHNllsmlyNzPHdeaQZuHmJn72zxJTroVlE0mrnaEz-L-Bx91ouB78i5ET6N2Q_hw6N8HnagLfcjx_vkXn9bDNvb5dTTqlAv07fQBpvdHzGGkAPEKyo-t_w</recordid><startdate>20110401</startdate><enddate>20110401</enddate><creator>Cheng, Xiang</creator><creator>Taleb, Soraya</creator><creator>Wang, Jun</creator><creator>Tang, Ting-Ting</creator><creator>Chen, Jian</creator><creator>Gao, Xing-Li</creator><creator>Yao, Rui</creator><creator>Xie, Jiang-Jiao</creator><creator>Yu, Xian</creator><creator>Xia, Ni</creator><creator>Yan, Xin-Xin</creator><creator>Nie, Shao-Fang</creator><creator>Liao, Meng-Yang</creator><creator>Cheng, Yan</creator><creator>Mallat, Ziad</creator><creator>Liao, Yu-Hua</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>FBQ</scope><scope>IQODW</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></search><sort><creationdate>20110401</creationdate><title>Inhibition of IL-17A in atherosclerosis</title><author>Cheng, Xiang ; Taleb, Soraya ; Wang, Jun ; Tang, Ting-Ting ; Chen, Jian ; Gao, Xing-Li ; Yao, Rui ; Xie, Jiang-Jiao ; Yu, Xian ; Xia, Ni ; Yan, Xin-Xin ; Nie, Shao-Fang ; Liao, Meng-Yang ; Cheng, Yan ; Mallat, Ziad ; Liao, Yu-Hua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c497t-8f5beac2e186b616b7acd0bcdcb0dc1b1cd1c1aa0e0396185d9db8c8cca237d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>antibodies</topic><topic>Antibodies - pharmacology</topic><topic>Antibody</topic><topic>Apolipoproteins E - deficiency</topic><topic>Associated diseases and complications</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Atherosclerosis - immunology</topic><topic>Atherosclerosis - prevention & control</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>bone marrow</topic><topic>bone marrow cells</topic><topic>Bone marrow transplantation</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>IL-17A</topic><topic>Inflammation</topic><topic>Interleukin-17 - antagonists & inhibitors</topic><topic>Interleukin-17 - immunology</topic><topic>Interleukin-17 - physiology</topic><topic>interleukins</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Plaque, Atherosclerotic - prevention & control</topic><topic>Rats</topic><topic>Receptors, LDL - deficiency</topic><topic>Signal Transduction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheng, Xiang</creatorcontrib><creatorcontrib>Taleb, Soraya</creatorcontrib><creatorcontrib>Wang, Jun</creatorcontrib><creatorcontrib>Tang, Ting-Ting</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>Gao, Xing-Li</creatorcontrib><creatorcontrib>Yao, Rui</creatorcontrib><creatorcontrib>Xie, Jiang-Jiao</creatorcontrib><creatorcontrib>Yu, Xian</creatorcontrib><creatorcontrib>Xia, Ni</creatorcontrib><creatorcontrib>Yan, Xin-Xin</creatorcontrib><creatorcontrib>Nie, Shao-Fang</creatorcontrib><creatorcontrib>Liao, Meng-Yang</creatorcontrib><creatorcontrib>Cheng, Yan</creatorcontrib><creatorcontrib>Mallat, Ziad</creatorcontrib><creatorcontrib>Liao, Yu-Hua</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</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><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheng, Xiang</au><au>Taleb, Soraya</au><au>Wang, Jun</au><au>Tang, Ting-Ting</au><au>Chen, Jian</au><au>Gao, Xing-Li</au><au>Yao, Rui</au><au>Xie, Jiang-Jiao</au><au>Yu, Xian</au><au>Xia, Ni</au><au>Yan, Xin-Xin</au><au>Nie, Shao-Fang</au><au>Liao, Meng-Yang</au><au>Cheng, Yan</au><au>Mallat, Ziad</au><au>Liao, Yu-Hua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of IL-17A in atherosclerosis</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2011-04-01</date><risdate>2011</risdate><volume>215</volume><issue>2</issue><spage>471</spage><epage>474</epage><pages>471-474</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Abstract Objective To determine the effects of interleukin (IL)-17A inhibition on experimental atherosclerosis. Methods and results ApoE−/− mice were treated with either rat anti-mouse IL-17A, mouse anti-mouse IL-17A or isotype-matched control antibodies for 12 weeks ( n = 8–10 per group). Ldlr−/− mice were transplanted with IL-17A-deficient or wild type bone marrow ( n = 8 per group). Rat anti-mouse IL-17A treatment obviously reduced plaque size by 43% ( p < 0.01) without evidence of reduced IL-17A signaling. In contrast, mouse anti-mouse IL-17A treatment and IL-17A deficiency in bone marrow cells did not alter lesion size despite significant reduction of IL-17A production. Conclusions Inhibition of IL-17A signaling does not alter lesion development in Th1-biased C57BL/6 ApoE−/− and Ldlr−/− mice with already low levels of IL-17A production. Alteration of lesion development after repeated injections of rat anti-mouse IL-17A antibody in ApoE−/− mice could not be attributed to blockade of IL-17A signaling.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>21300351</pmid><doi>10.1016/j.atherosclerosis.2010.12.034</doi><tpages>4</tpages></addata></record> |
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| subjects | Animals antibodies Antibodies - pharmacology Antibody Apolipoproteins E - deficiency Associated diseases and complications Atherosclerosis Atherosclerosis (general aspects, experimental research) Atherosclerosis - immunology Atherosclerosis - prevention & control Biological and medical sciences Blood and lymphatic vessels bone marrow bone marrow cells Bone marrow transplantation Cardiology. Vascular system Cardiovascular Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Female IL-17A Inflammation Interleukin-17 - antagonists & inhibitors Interleukin-17 - immunology Interleukin-17 - physiology interleukins Male Medical sciences Mice Mice, Inbred C57BL Plaque, Atherosclerotic - prevention & control Rats Receptors, LDL - deficiency Signal Transduction - drug effects |
| title | Inhibition of IL-17A in atherosclerosis |
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