Epigenetic mechanisms and the development of asthma
Asthma is heritable, influenced by the environment, and modified by in utero exposures and aging; all of these features are also common to epigenetic regulation. Furthermore, the transcription factors that are involved in the development of mature T cells that are critical to the TH 2 immune phenoty...
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| Veröffentlicht in: | Journal of allergy and clinical immunology 2012-12, Vol.130 (6), p.1243-1255 |
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| description | Asthma is heritable, influenced by the environment, and modified by in utero exposures and aging; all of these features are also common to epigenetic regulation. Furthermore, the transcription factors that are involved in the development of mature T cells that are critical to the TH 2 immune phenotype in asthmatic patients are regulated by epigenetic mechanisms. Epigenetic marks (DNA methylation, modifications of histone tails, and noncoding RNAs) work in concert with other components of the cellular regulatory machinery to control the spatial and temporal levels of expressed genes. Technology to measure epigenetic marks on a genomic scale and comprehensive approaches to data analysis have recently emerged and continue to improve. Alterations in epigenetic marks have been associated with exposures relevant to asthma, particularly air pollution and tobacco smoke, as well as asthma phenotypes, in a few population-based studies. On the other hand, animal studies have begun to decipher the role of epigenetic regulation of gene expression associated with the development of allergic airway disease. Epigenetic mechanisms represent a promising line of inquiry that might, in part, explain the inheritance and immunobiology of asthma. |
| doi_str_mv | 10.1016/j.jaci.2012.07.052 |
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Furthermore, the transcription factors that are involved in the development of mature T cells that are critical to the TH 2 immune phenotype in asthmatic patients are regulated by epigenetic mechanisms. Epigenetic marks (DNA methylation, modifications of histone tails, and noncoding RNAs) work in concert with other components of the cellular regulatory machinery to control the spatial and temporal levels of expressed genes. Technology to measure epigenetic marks on a genomic scale and comprehensive approaches to data analysis have recently emerged and continue to improve. Alterations in epigenetic marks have been associated with exposures relevant to asthma, particularly air pollution and tobacco smoke, as well as asthma phenotypes, in a few population-based studies. On the other hand, animal studies have begun to decipher the role of epigenetic regulation of gene expression associated with the development of allergic airway disease. Epigenetic mechanisms represent a promising line of inquiry that might, in part, explain the inheritance and immunobiology of asthma.</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/j.jaci.2012.07.052</identifier><identifier>PMID: 23026498</identifier><identifier>CODEN: JACIBY</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Aging ; Air pollution ; Allergies ; Allergy and Immunology ; Animals ; Asthma ; Asthma - genetics ; Asthma - immunology ; atopy ; Biological and medical sciences ; Chronic obstructive pulmonary disease, asthma ; Data processing ; Deoxyribonucleic acid ; DNA ; DNA methylation ; Epigenesis, Genetic ; Epigenetics ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Gene expression ; Gene regulation ; Gene Regulatory Networks ; Genetics ; Genomes ; Genomics ; Helper cells ; Heredity ; histone marks ; Histones ; Humans ; Immunopathology ; Lymphocytes T ; Machinery ; Medical sciences ; Mortality ; Mutation ; noncoding RNAs ; Pneumology ; Polycyclic aromatic hydrocarbons ; Population studies ; Prenatal experience ; Proteins ; Respiratory diseases ; Respiratory tract diseases ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Smoke ; T-Lymphocyte Subsets - immunology ; Th2 Cells - immunology ; Tobacco ; Transcription ; Transcription factors</subject><ispartof>Journal of allergy and clinical immunology, 2012-12, Vol.130 (6), p.1243-1255</ispartof><rights>American Academy of Allergy, Asthma & Immunology</rights><rights>2012 American Academy of Allergy, Asthma & Immunology</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2012 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Dec 2012</rights><rights>2012 American Academy of Allergy, Asthma and Immunology. Published by Mosby, Inc. All rights reserved. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c650t-d96dba48381ca8738e9525b6908343227072594a619fa30a4a07f079507cec673</citedby><cites>FETCH-LOGICAL-c650t-d96dba48381ca8738e9525b6908343227072594a619fa30a4a07f079507cec673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0091674912013048$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26726818$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23026498$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Ivana V., PhD</creatorcontrib><creatorcontrib>Schwartz, David A., MD</creatorcontrib><title>Epigenetic mechanisms and the development of asthma</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>Asthma is heritable, influenced by the environment, and modified by in utero exposures and aging; all of these features are also common to epigenetic regulation. Furthermore, the transcription factors that are involved in the development of mature T cells that are critical to the TH 2 immune phenotype in asthmatic patients are regulated by epigenetic mechanisms. Epigenetic marks (DNA methylation, modifications of histone tails, and noncoding RNAs) work in concert with other components of the cellular regulatory machinery to control the spatial and temporal levels of expressed genes. Technology to measure epigenetic marks on a genomic scale and comprehensive approaches to data analysis have recently emerged and continue to improve. Alterations in epigenetic marks have been associated with exposures relevant to asthma, particularly air pollution and tobacco smoke, as well as asthma phenotypes, in a few population-based studies. On the other hand, animal studies have begun to decipher the role of epigenetic regulation of gene expression associated with the development of allergic airway disease. Epigenetic mechanisms represent a promising line of inquiry that might, in part, explain the inheritance and immunobiology of asthma.</description><subject>Aging</subject><subject>Air pollution</subject><subject>Allergies</subject><subject>Allergy and Immunology</subject><subject>Animals</subject><subject>Asthma</subject><subject>Asthma - genetics</subject><subject>Asthma - immunology</subject><subject>atopy</subject><subject>Biological and medical sciences</subject><subject>Chronic obstructive pulmonary disease, asthma</subject><subject>Data processing</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Gene Regulatory Networks</subject><subject>Genetics</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Helper cells</subject><subject>Heredity</subject><subject>histone marks</subject><subject>Histones</subject><subject>Humans</subject><subject>Immunopathology</subject><subject>Lymphocytes T</subject><subject>Machinery</subject><subject>Medical sciences</subject><subject>Mortality</subject><subject>Mutation</subject><subject>noncoding RNAs</subject><subject>Pneumology</subject><subject>Polycyclic aromatic hydrocarbons</subject><subject>Population studies</subject><subject>Prenatal experience</subject><subject>Proteins</subject><subject>Respiratory diseases</subject><subject>Respiratory tract diseases</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Smoke</subject><subject>T-Lymphocyte Subsets - immunology</subject><subject>Th2 Cells - immunology</subject><subject>Tobacco</subject><subject>Transcription</subject><subject>Transcription factors</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkl1rFDEUhoModq3-AS9kQARvZjz5mHyAFEppVSh4oV6HbOZMN-N8rMnsQv-9GXbbai9EchFCnvfNOecNIa8pVBSo_NBVnfOhYkBZBaqCmj0hKwpGlVKz-ilZARhaSiXMCXmRUgf5zLV5Tk4YByaF0SvCL7fhBkecgy8G9Bs3hjSkwo1NMW-waHCP_bQdcJyLqS1cmjeDe0meta5P-Oq4n5IfV5ffLz6X118_fbk4vy69rGEuGyObtROaa-qdVlyjqVm9lgY0F5wxBYrVRjhJTes4OOFAtaBMDcqjl4qfkrOD73a3HrDxuYjoeruNYXDx1k4u2L9vxrCxN9Pe8ppqrkQ2eH80iNOvHabZDiF57Hs34rRLljKVFwOl_wNllGZfDhl9-wjtpl0c8yQsrUFoJgSwTLED5eOUUsT2vm4KdonPdnaJzy7xWVA2x5dFb_7s-F5yl1cG3h0Bl7zr2-hGH9IDJxWTmi7cxwOHOZ99wGiTDzh6bEJEP9tmCv-u4-yR3PdhDPnFn3iL6aFfm7LGfls-2vLPaDbheQT8N0-9yn4</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Yang, Ivana V., PhD</creator><creator>Schwartz, David A., MD</creator><general>Mosby, Inc</general><general>Elsevier</general><general>Elsevier Limited</general><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>7SS</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>7T2</scope><scope>7TM</scope><scope>7U2</scope><scope>C1K</scope><scope>5PM</scope></search><sort><creationdate>20121201</creationdate><title>Epigenetic mechanisms and the development of asthma</title><author>Yang, Ivana V., PhD ; Schwartz, David A., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c650t-d96dba48381ca8738e9525b6908343227072594a619fa30a4a07f079507cec673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Aging</topic><topic>Air pollution</topic><topic>Allergies</topic><topic>Allergy and Immunology</topic><topic>Animals</topic><topic>Asthma</topic><topic>Asthma - genetics</topic><topic>Asthma - immunology</topic><topic>atopy</topic><topic>Biological and medical sciences</topic><topic>Chronic obstructive pulmonary disease, asthma</topic><topic>Data processing</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA methylation</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>Gene Regulatory Networks</topic><topic>Genetics</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Helper cells</topic><topic>Heredity</topic><topic>histone marks</topic><topic>Histones</topic><topic>Humans</topic><topic>Immunopathology</topic><topic>Lymphocytes T</topic><topic>Machinery</topic><topic>Medical sciences</topic><topic>Mortality</topic><topic>Mutation</topic><topic>noncoding RNAs</topic><topic>Pneumology</topic><topic>Polycyclic aromatic hydrocarbons</topic><topic>Population studies</topic><topic>Prenatal experience</topic><topic>Proteins</topic><topic>Respiratory diseases</topic><topic>Respiratory tract diseases</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>Smoke</topic><topic>T-Lymphocyte Subsets - immunology</topic><topic>Th2 Cells - immunology</topic><topic>Tobacco</topic><topic>Transcription</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Ivana V., PhD</creatorcontrib><creatorcontrib>Schwartz, David A., MD</creatorcontrib><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>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Nucleic Acids Abstracts</collection><collection>Safety Science and Risk</collection><collection>Environmental Sciences and Pollution Management</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of allergy and clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Ivana V., PhD</au><au>Schwartz, David A., MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epigenetic mechanisms and the development of asthma</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>2012-12-01</date><risdate>2012</risdate><volume>130</volume><issue>6</issue><spage>1243</spage><epage>1255</epage><pages>1243-1255</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><coden>JACIBY</coden><abstract>Asthma is heritable, influenced by the environment, and modified by in utero exposures and aging; all of these features are also common to epigenetic regulation. Furthermore, the transcription factors that are involved in the development of mature T cells that are critical to the TH 2 immune phenotype in asthmatic patients are regulated by epigenetic mechanisms. Epigenetic marks (DNA methylation, modifications of histone tails, and noncoding RNAs) work in concert with other components of the cellular regulatory machinery to control the spatial and temporal levels of expressed genes. Technology to measure epigenetic marks on a genomic scale and comprehensive approaches to data analysis have recently emerged and continue to improve. Alterations in epigenetic marks have been associated with exposures relevant to asthma, particularly air pollution and tobacco smoke, as well as asthma phenotypes, in a few population-based studies. On the other hand, animal studies have begun to decipher the role of epigenetic regulation of gene expression associated with the development of allergic airway disease. Epigenetic mechanisms represent a promising line of inquiry that might, in part, explain the inheritance and immunobiology of asthma.</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>23026498</pmid><doi>10.1016/j.jaci.2012.07.052</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of allergy and clinical immunology, 2012-12, Vol.130 (6), p.1243-1255 |
| issn | 0091-6749 1097-6825 |
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| subjects | Aging Air pollution Allergies Allergy and Immunology Animals Asthma Asthma - genetics Asthma - immunology atopy Biological and medical sciences Chronic obstructive pulmonary disease, asthma Data processing Deoxyribonucleic acid DNA DNA methylation Epigenesis, Genetic Epigenetics Fundamental and applied biological sciences. Psychology Fundamental immunology Gene expression Gene regulation Gene Regulatory Networks Genetics Genomes Genomics Helper cells Heredity histone marks Histones Humans Immunopathology Lymphocytes T Machinery Medical sciences Mortality Mutation noncoding RNAs Pneumology Polycyclic aromatic hydrocarbons Population studies Prenatal experience Proteins Respiratory diseases Respiratory tract diseases Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Smoke T-Lymphocyte Subsets - immunology Th2 Cells - immunology Tobacco Transcription Transcription factors |
| title | Epigenetic mechanisms and the development of asthma |
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