Increase of angiotensin II type 1 receptor auto-antibodies in Huntington's disease
In the recent years, a role of the immune system in Huntington's disease (HD) is increasingly recognized. Here we investigate the presence of T cell activating auto-antibodies against angiotensin II type 1 receptors (AT1R) in all stages of the disease as compared to healthy controls and patient...
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| Veröffentlicht in: | Molecular neurodegeneration 2014-11, Vol.9 (1), p.49-49, Article 49 |
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| creator | Lee, De-Hyung Heidecke, Harald Schröder, Alexandra Paul, Friedemann Wachter, Rolf Hoffmann, Rainer Ellrichmann, Gisa Dragun, Duska Waschbisch, Anne Stegbauer, Johannes Klotz, Peter Gold, Ralf Dechend, Ralf Müller, Dominik N Saft, Carsten Linker, Ralf A |
| description | In the recent years, a role of the immune system in Huntington's disease (HD) is increasingly recognized. Here we investigate the presence of T cell activating auto-antibodies against angiotensin II type 1 receptors (AT1R) in all stages of the disease as compared to healthy controls and patients suffering from multiple sclerosis (MS) as a prototype neurologic autoimmune disease.
As compared to controls, MS patients show higher titers of anti-AT1R antibodies, especially in individuals with active disease. In HD, anti-AT1R antibodies are more frequent than in healthy controls or even MS and occur in 37.9% of patients with relevant titers ≥ 20 U/ml. In a correlation analysis with clinical parameters, the presence of AT1R antibodies in the sera of HD individuals inversely correlated with the age of onset and positively with the disease burden score as well as with smoking and infection.
These data suggest a dysfunction of the adaptive immune system in HD which may be triggered by different stimuli including autoimmune responses, infection and possibly also smoking. |
| doi_str_mv | 10.1186/1750-1326-9-49 |
| format | Article |
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As compared to controls, MS patients show higher titers of anti-AT1R antibodies, especially in individuals with active disease. In HD, anti-AT1R antibodies are more frequent than in healthy controls or even MS and occur in 37.9% of patients with relevant titers ≥ 20 U/ml. In a correlation analysis with clinical parameters, the presence of AT1R antibodies in the sera of HD individuals inversely correlated with the age of onset and positively with the disease burden score as well as with smoking and infection.
These data suggest a dysfunction of the adaptive immune system in HD which may be triggered by different stimuli including autoimmune responses, infection and possibly also smoking.</description><identifier>ISSN: 1750-1326</identifier><identifier>EISSN: 1750-1326</identifier><identifier>DOI: 10.1186/1750-1326-9-49</identifier><identifier>PMID: 25398321</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Acquisitions & mergers ; Adult ; Aged ; Aged, 80 and over ; Analysis ; Angiotensin ; Autoantibodies ; Autoantibodies - immunology ; Autoantigens - immunology ; Autoimmunity ; Comparative analysis ; Compensation ; Drug therapy ; Enzyme-Linked Immunosorbent Assay ; Female ; Health aspects ; High-definition television ; Humans ; Huntington Disease - immunology ; Huntingtons disease ; Immune system ; Male ; Middle Aged ; Mortality ; Multiple sclerosis ; Nephrology ; Neurology ; NMR ; Nuclear magnetic resonance ; Pathogenesis ; Pharmaceutical industry ; Receptor, Angiotensin, Type 1 - immunology ; Risk assessment ; Statistical analysis ; Young Adult</subject><ispartof>Molecular neurodegeneration, 2014-11, Vol.9 (1), p.49-49, Article 49</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>2014 Lee et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Lee et al.; licensee BioMed Central Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c518t-2b17554ac88bfa4c7b21247ced47abea1309ce1bc5149bfada25ea6906c51e8e3</citedby><cites>FETCH-LOGICAL-c518t-2b17554ac88bfa4c7b21247ced47abea1309ce1bc5149bfada25ea6906c51e8e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246494/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246494/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25398321$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, De-Hyung</creatorcontrib><creatorcontrib>Heidecke, Harald</creatorcontrib><creatorcontrib>Schröder, Alexandra</creatorcontrib><creatorcontrib>Paul, Friedemann</creatorcontrib><creatorcontrib>Wachter, Rolf</creatorcontrib><creatorcontrib>Hoffmann, Rainer</creatorcontrib><creatorcontrib>Ellrichmann, Gisa</creatorcontrib><creatorcontrib>Dragun, Duska</creatorcontrib><creatorcontrib>Waschbisch, Anne</creatorcontrib><creatorcontrib>Stegbauer, Johannes</creatorcontrib><creatorcontrib>Klotz, Peter</creatorcontrib><creatorcontrib>Gold, Ralf</creatorcontrib><creatorcontrib>Dechend, Ralf</creatorcontrib><creatorcontrib>Müller, Dominik N</creatorcontrib><creatorcontrib>Saft, Carsten</creatorcontrib><creatorcontrib>Linker, Ralf A</creatorcontrib><title>Increase of angiotensin II type 1 receptor auto-antibodies in Huntington's disease</title><title>Molecular neurodegeneration</title><addtitle>Mol Neurodegener</addtitle><description>In the recent years, a role of the immune system in Huntington's disease (HD) is increasingly recognized. Here we investigate the presence of T cell activating auto-antibodies against angiotensin II type 1 receptors (AT1R) in all stages of the disease as compared to healthy controls and patients suffering from multiple sclerosis (MS) as a prototype neurologic autoimmune disease.
As compared to controls, MS patients show higher titers of anti-AT1R antibodies, especially in individuals with active disease. In HD, anti-AT1R antibodies are more frequent than in healthy controls or even MS and occur in 37.9% of patients with relevant titers ≥ 20 U/ml. In a correlation analysis with clinical parameters, the presence of AT1R antibodies in the sera of HD individuals inversely correlated with the age of onset and positively with the disease burden score as well as with smoking and infection.
These data suggest a dysfunction of the adaptive immune system in HD which may be triggered by different stimuli including autoimmune responses, infection and possibly also smoking.</description><subject>Acquisitions & mergers</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Analysis</subject><subject>Angiotensin</subject><subject>Autoantibodies</subject><subject>Autoantibodies - immunology</subject><subject>Autoantigens - immunology</subject><subject>Autoimmunity</subject><subject>Comparative analysis</subject><subject>Compensation</subject><subject>Drug therapy</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Health aspects</subject><subject>High-definition television</subject><subject>Humans</subject><subject>Huntington Disease - immunology</subject><subject>Huntingtons disease</subject><subject>Immune system</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mortality</subject><subject>Multiple sclerosis</subject><subject>Nephrology</subject><subject>Neurology</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>Pathogenesis</subject><subject>Pharmaceutical industry</subject><subject>Receptor, Angiotensin, Type 1 - 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immunology</topic><topic>Autoantigens - immunology</topic><topic>Autoimmunity</topic><topic>Comparative analysis</topic><topic>Compensation</topic><topic>Drug therapy</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Health aspects</topic><topic>High-definition television</topic><topic>Humans</topic><topic>Huntington Disease - immunology</topic><topic>Huntingtons disease</topic><topic>Immune system</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mortality</topic><topic>Multiple sclerosis</topic><topic>Nephrology</topic><topic>Neurology</topic><topic>NMR</topic><topic>Nuclear magnetic resonance</topic><topic>Pathogenesis</topic><topic>Pharmaceutical industry</topic><topic>Receptor, Angiotensin, Type 1 - immunology</topic><topic>Risk assessment</topic><topic>Statistical analysis</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, De-Hyung</creatorcontrib><creatorcontrib>Heidecke, Harald</creatorcontrib><creatorcontrib>Schröder, Alexandra</creatorcontrib><creatorcontrib>Paul, Friedemann</creatorcontrib><creatorcontrib>Wachter, Rolf</creatorcontrib><creatorcontrib>Hoffmann, Rainer</creatorcontrib><creatorcontrib>Ellrichmann, Gisa</creatorcontrib><creatorcontrib>Dragun, Duska</creatorcontrib><creatorcontrib>Waschbisch, Anne</creatorcontrib><creatorcontrib>Stegbauer, Johannes</creatorcontrib><creatorcontrib>Klotz, Peter</creatorcontrib><creatorcontrib>Gold, Ralf</creatorcontrib><creatorcontrib>Dechend, Ralf</creatorcontrib><creatorcontrib>Müller, Dominik N</creatorcontrib><creatorcontrib>Saft, Carsten</creatorcontrib><creatorcontrib>Linker, Ralf A</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>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Publicly Available Content 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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular neurodegeneration</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, De-Hyung</au><au>Heidecke, Harald</au><au>Schröder, Alexandra</au><au>Paul, Friedemann</au><au>Wachter, Rolf</au><au>Hoffmann, Rainer</au><au>Ellrichmann, Gisa</au><au>Dragun, Duska</au><au>Waschbisch, Anne</au><au>Stegbauer, Johannes</au><au>Klotz, Peter</au><au>Gold, Ralf</au><au>Dechend, Ralf</au><au>Müller, Dominik N</au><au>Saft, Carsten</au><au>Linker, Ralf A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increase of angiotensin II type 1 receptor auto-antibodies in Huntington's disease</atitle><jtitle>Molecular neurodegeneration</jtitle><addtitle>Mol Neurodegener</addtitle><date>2014-11-15</date><risdate>2014</risdate><volume>9</volume><issue>1</issue><spage>49</spage><epage>49</epage><pages>49-49</pages><artnum>49</artnum><issn>1750-1326</issn><eissn>1750-1326</eissn><abstract>In the recent years, a role of the immune system in Huntington's disease (HD) is increasingly recognized. Here we investigate the presence of T cell activating auto-antibodies against angiotensin II type 1 receptors (AT1R) in all stages of the disease as compared to healthy controls and patients suffering from multiple sclerosis (MS) as a prototype neurologic autoimmune disease.
As compared to controls, MS patients show higher titers of anti-AT1R antibodies, especially in individuals with active disease. In HD, anti-AT1R antibodies are more frequent than in healthy controls or even MS and occur in 37.9% of patients with relevant titers ≥ 20 U/ml. In a correlation analysis with clinical parameters, the presence of AT1R antibodies in the sera of HD individuals inversely correlated with the age of onset and positively with the disease burden score as well as with smoking and infection.
These data suggest a dysfunction of the adaptive immune system in HD which may be triggered by different stimuli including autoimmune responses, infection and possibly also smoking.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>25398321</pmid><doi>10.1186/1750-1326-9-49</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acquisitions & mergers Adult Aged Aged, 80 and over Analysis Angiotensin Autoantibodies Autoantibodies - immunology Autoantigens - immunology Autoimmunity Comparative analysis Compensation Drug therapy Enzyme-Linked Immunosorbent Assay Female Health aspects High-definition television Humans Huntington Disease - immunology Huntingtons disease Immune system Male Middle Aged Mortality Multiple sclerosis Nephrology Neurology NMR Nuclear magnetic resonance Pathogenesis Pharmaceutical industry Receptor, Angiotensin, Type 1 - immunology Risk assessment Statistical analysis Young Adult |
| title | Increase of angiotensin II type 1 receptor auto-antibodies in Huntington's disease |
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