Mechanisms underlying helper T-cell plasticity: Implications for immune-mediated disease
CD4 helper T cells are critical for proper immune cell homeostasis and host defense but are also major contributors to immune and inflammatory disease. Arising from a simple biphasic model of differentiation (ie, TH 1 and TH 2 cells). A bewildering number of fates seem possible for helper T cells. T...
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| Veröffentlicht in: | Journal of allergy and clinical immunology 2013-05, Vol.131 (5), p.1276-1287 |
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| container_title | Journal of allergy and clinical immunology |
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| creator | Hirahara, Kiyoshi, MD, PhD Poholek, Amanda, PhD Vahedi, Golnaz, PhD Laurence, Arian, PhD, MRCP, FRCPath Kanno, Yuka, MD, PhD Milner, Joshua D., MD O’Shea, John J., MD |
| description | CD4 helper T cells are critical for proper immune cell homeostasis and host defense but are also major contributors to immune and inflammatory disease. Arising from a simple biphasic model of differentiation (ie, TH 1 and TH 2 cells). A bewildering number of fates seem possible for helper T cells. To what extent different helper cell subsets maintain their characteristic gene expression profiles or exhibit functional plasticity is a hotly debated topic. In this review we will discuss how the expression of “signature cytokines” and “master regulator” transcription factors do not neatly conform to a simple helper T-cell paradigm. Although this might seem confusing, the good news is that the newly recognized complexity fits better with our understanding of immunopathogenesis. Finally, we will discuss factors, including epigenetic regulation and metabolic alterations, that contribute to helper cell specificity and plasticity. |
| doi_str_mv | 10.1016/j.jaci.2013.03.015 |
| format | Article |
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Arising from a simple biphasic model of differentiation (ie, TH 1 and TH 2 cells). A bewildering number of fates seem possible for helper T cells. To what extent different helper cell subsets maintain their characteristic gene expression profiles or exhibit functional plasticity is a hotly debated topic. In this review we will discuss how the expression of “signature cytokines” and “master regulator” transcription factors do not neatly conform to a simple helper T-cell paradigm. Although this might seem confusing, the good news is that the newly recognized complexity fits better with our understanding of immunopathogenesis. Finally, we will discuss factors, including epigenetic regulation and metabolic alterations, that contribute to helper cell specificity and plasticity.</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/j.jaci.2013.03.015</identifier><identifier>PMID: 23622118</identifier><identifier>CODEN: JACIBY</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>allergic disease ; Allergy and Immunology ; Asthma ; Binding sites ; Biological and medical sciences ; Biology ; Chronic obstructive pulmonary disease, asthma ; Cytokines - biosynthesis ; Cytokines - genetics ; Deoxyribonucleic acid ; Disease ; DNA ; Epigenetics ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Gene expression ; Gene Expression Regulation - immunology ; Genomes ; histone modification ; Humans ; Immune system ; Immune System Diseases - etiology ; Immune System Diseases - immunology ; Immune System Diseases - pathology ; Immunopathology ; Influence ; Kinases ; Ligands ; Lymphocytes ; Medical sciences ; Metabolism ; Models, Immunological ; Mutation ; Pneumology ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Studies ; T-cell plasticity ; T-Lymphocytes, Helper-Inducer - immunology ; T-Lymphocytes, Helper-Inducer - metabolism ; T-Lymphocytes, Helper-Inducer - pathology ; therapy ; Transcription factors</subject><ispartof>Journal of allergy and clinical immunology, 2013-05, Vol.131 (5), p.1276-1287</ispartof><rights>2013</rights><rights>2014 INIST-CNRS</rights><rights>Published by Mosby, Inc.</rights><rights>Copyright Elsevier Limited May 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c601t-c1e6ae61e3b510e10afd06894477743870cc3e98b908d4cfc6bc38c36d0365393</citedby><cites>FETCH-LOGICAL-c601t-c1e6ae61e3b510e10afd06894477743870cc3e98b908d4cfc6bc38c36d0365393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jaci.2013.03.015$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27321861$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23622118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirahara, Kiyoshi, MD, PhD</creatorcontrib><creatorcontrib>Poholek, Amanda, PhD</creatorcontrib><creatorcontrib>Vahedi, Golnaz, PhD</creatorcontrib><creatorcontrib>Laurence, Arian, PhD, MRCP, FRCPath</creatorcontrib><creatorcontrib>Kanno, Yuka, MD, PhD</creatorcontrib><creatorcontrib>Milner, Joshua D., MD</creatorcontrib><creatorcontrib>O’Shea, John J., MD</creatorcontrib><title>Mechanisms underlying helper T-cell plasticity: Implications for immune-mediated disease</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>CD4 helper T cells are critical for proper immune cell homeostasis and host defense but are also major contributors to immune and inflammatory disease. Arising from a simple biphasic model of differentiation (ie, TH 1 and TH 2 cells). A bewildering number of fates seem possible for helper T cells. To what extent different helper cell subsets maintain their characteristic gene expression profiles or exhibit functional plasticity is a hotly debated topic. In this review we will discuss how the expression of “signature cytokines” and “master regulator” transcription factors do not neatly conform to a simple helper T-cell paradigm. Although this might seem confusing, the good news is that the newly recognized complexity fits better with our understanding of immunopathogenesis. Finally, we will discuss factors, including epigenetic regulation and metabolic alterations, that contribute to helper cell specificity and plasticity.</description><subject>allergic disease</subject><subject>Allergy and Immunology</subject><subject>Asthma</subject><subject>Binding sites</subject><subject>Biological and medical sciences</subject><subject>Biology</subject><subject>Chronic obstructive pulmonary disease, asthma</subject><subject>Cytokines - biosynthesis</subject><subject>Cytokines - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>Disease</subject><subject>DNA</subject><subject>Epigenetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - immunology</subject><subject>Genomes</subject><subject>histone modification</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immune System Diseases - etiology</subject><subject>Immune System Diseases - immunology</subject><subject>Immune System Diseases - pathology</subject><subject>Immunopathology</subject><subject>Influence</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Lymphocytes</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Models, Immunological</subject><subject>Mutation</subject><subject>Pneumology</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Studies</subject><subject>T-cell plasticity</subject><subject>T-Lymphocytes, Helper-Inducer - immunology</subject><subject>T-Lymphocytes, Helper-Inducer - metabolism</subject><subject>T-Lymphocytes, Helper-Inducer - pathology</subject><subject>therapy</subject><subject>Transcription factors</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkk9r3DAQxU1paTZpv0APxVAKvXg7Y9myXUqghP4JpPTQFHoT2vE4q60sbyQ7sN8-MrtN2hxKQSCEfjN6T2-S5AXCEgHl281yo8ksc0CxhLiwfJQsEJoqk3VePk4WAA1msiqao-Q4hA3Es6ibp8lRLmSeI9aL5OdXprV2JvQhnVzL3u6Mu0rXbLfs08uM2Np0a3UYDZlx9y4977fWkB7N4ELaDT41fT85znpujR65TVsTWAd-ljzptA38_LCfJD8-fbw8-5JdfPt8fvbhIiMJOGaELDVLZLEqERhBdy3IuimKqqoKUVdAJLipVw3UbUEdyRWJmoRsQchSNOIkOd333U6rqIHYjV5btfWm136nBm3U3zfOrNXVcKOEnF-oY4M3hwZ-uJ44jKo3YbatHQ9TUCiqHEoRNf0HWlR52UBRRfTVA3QzTN7Fn1Aoo7lotigile8p8kMInrs73Qhqzlht1JyxmjNWEBeWsejln47vSn6HGoHXB0AH0rbz2pEJ91wlcqwlRu79nuOYz41hrwIZdhST9Eyjagfzbx2nD8rJGhdnw_7iHYd7vyrkCtT3eRrnYUQBUIIoxC2KHdmr</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Hirahara, Kiyoshi, MD, PhD</creator><creator>Poholek, Amanda, PhD</creator><creator>Vahedi, Golnaz, PhD</creator><creator>Laurence, Arian, PhD, MRCP, FRCPath</creator><creator>Kanno, Yuka, MD, PhD</creator><creator>Milner, Joshua D., MD</creator><creator>O’Shea, John J., 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>5PM</scope></search><sort><creationdate>20130501</creationdate><title>Mechanisms underlying helper T-cell plasticity: Implications for immune-mediated disease</title><author>Hirahara, Kiyoshi, MD, PhD ; Poholek, Amanda, PhD ; Vahedi, Golnaz, PhD ; Laurence, Arian, PhD, MRCP, FRCPath ; Kanno, Yuka, MD, PhD ; Milner, Joshua D., MD ; O’Shea, John J., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c601t-c1e6ae61e3b510e10afd06894477743870cc3e98b908d4cfc6bc38c36d0365393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>allergic disease</topic><topic>Allergy and Immunology</topic><topic>Asthma</topic><topic>Binding sites</topic><topic>Biological and medical sciences</topic><topic>Biology</topic><topic>Chronic obstructive pulmonary disease, asthma</topic><topic>Cytokines - biosynthesis</topic><topic>Cytokines - genetics</topic><topic>Deoxyribonucleic acid</topic><topic>Disease</topic><topic>DNA</topic><topic>Epigenetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - immunology</topic><topic>Genomes</topic><topic>histone modification</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immune System Diseases - etiology</topic><topic>Immune System Diseases - immunology</topic><topic>Immune System Diseases - pathology</topic><topic>Immunopathology</topic><topic>Influence</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Lymphocytes</topic><topic>Medical sciences</topic><topic>Metabolism</topic><topic>Models, Immunological</topic><topic>Mutation</topic><topic>Pneumology</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. 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Arising from a simple biphasic model of differentiation (ie, TH 1 and TH 2 cells). A bewildering number of fates seem possible for helper T cells. To what extent different helper cell subsets maintain their characteristic gene expression profiles or exhibit functional plasticity is a hotly debated topic. In this review we will discuss how the expression of “signature cytokines” and “master regulator” transcription factors do not neatly conform to a simple helper T-cell paradigm. Although this might seem confusing, the good news is that the newly recognized complexity fits better with our understanding of immunopathogenesis. Finally, we will discuss factors, including epigenetic regulation and metabolic alterations, that contribute to helper cell specificity and plasticity.</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>23622118</pmid><doi>10.1016/j.jaci.2013.03.015</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of allergy and clinical immunology, 2013-05, Vol.131 (5), p.1276-1287 |
| issn | 0091-6749 1097-6825 |
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| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | allergic disease Allergy and Immunology Asthma Binding sites Biological and medical sciences Biology Chronic obstructive pulmonary disease, asthma Cytokines - biosynthesis Cytokines - genetics Deoxyribonucleic acid Disease DNA Epigenetics Fundamental and applied biological sciences. Psychology Fundamental immunology Gene expression Gene Expression Regulation - immunology Genomes histone modification Humans Immune system Immune System Diseases - etiology Immune System Diseases - immunology Immune System Diseases - pathology Immunopathology Influence Kinases Ligands Lymphocytes Medical sciences Metabolism Models, Immunological Mutation Pneumology Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Studies T-cell plasticity T-Lymphocytes, Helper-Inducer - immunology T-Lymphocytes, Helper-Inducer - metabolism T-Lymphocytes, Helper-Inducer - pathology therapy Transcription factors |
| title | Mechanisms underlying helper T-cell plasticity: Implications for immune-mediated disease |
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