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Verfasst von:Li-Weber, Min [VerfasserIn]   i
 Krammer, Peter H. [VerfasserIn]   i
Titel:Regulation of IL4 gene expression by T cells and therapeutic perspectives
Verf.angabe:Min Li-Weber and Peter H. Krammer
E-Jahr:2003
Jahr:01 July 2003
Umfang:10 S.
Teil:volume:3
 year:2003
 number:7
 month:07
 pages:534-543
 extent:10
Fussnoten:Gesehen am 02.03.2021
Titel Quelle:Enthalten in: Nature reviews / Immunology
Ort Quelle:London : Nature Publ. Group, 2001
Jahr Quelle:2003
Band/Heft Quelle:3(2003), 7 vom: Juli, Seite 534-543
ISSN Quelle:1474-1741
Abstract:Interleukin-4 (IL-4) is a key cytokine that controls the differentiation of T helper (TH) cells to the TH2 effector cells that are responsible for cellular immunity and inflammation.Expression of the gene encoding IL-4 by T cells is regulated in two steps — the early stages of T-cell differentiation and the later stage of acute gene expression by differentiated TH2 effector cells.During the first stage, the transcription factor GATA3 (GATA-binding protein 3), which is expressed during TH2-cell differentiation, induces chromatin remodelling at various control regions of the IL4 gene, leading to de-condensation of the IL4 locus.Acute expression of the IL4 gene by differentiated TH2 cells is regulated by many positive and negative inducible transcription factors, such as nuclear factor of activated T cells (NFAT) proteins, AP1, nuclear factor-κB, interferon regulatory factor 1 (IRF1) and other factors that bind the promoter and enhancer elements and coordinately achieve a fine degree of control over the transcriptional activity of the gene.As acute expression of IL-4 by TH2 effector cells has a central role in the pathogenesis of allergic diseases, a better understanding of the regulatory mechanisms for IL4 gene expression might provide greater possibilities to develop therapeutic strategies. Recently, studies with vitamin E, aspirin and parthenolide have shown the potential of intervening at the level of transcription of the IL4 gene.
DOI:doi:10.1038/nri1128
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1038/nri1128
 Volltext: https://www.nature.com/articles/nri1128
 DOI: https://doi.org/10.1038/nri1128
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1750143747
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