Systemic lupus erythematosus and epigenetics

dc.contributor.author	Ρέγκλη, Αρετή	el
dc.contributor.author	Κωνσταντινίδης, Πολύδωρος Ι.	el
dc.contributor.author	Μαλλής, Παναγιώτης	el
dc.contributor.author	Μάτσης, Κωνσταντίνος	el
dc.contributor.author	Κωνσταντινίδης, Ιωάννης	el
dc.date.accessioned	2015-01-29T07:44:37Z
dc.date.available	2015-01-29T07:44:37Z
dc.date.issued	2015-01-29
dc.identifier.uri	http://hdl.handle.net/11400/5000
dc.rights	Αναφορά Δημιουργού-Μη Εμπορική Χρήση-Όχι Παράγωγα Έργα 3.0 Ηνωμένες Πολιτείες	*
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/3.0/us/	*
dc.source	http://e-jst.teiath.gr/	en
dc.subject	Autoimmune inflammatory disease
dc.subject	Αυτοάνοση φλεγμονώδης νόσος
dc.subject	SLE
dc.subject	Epigenetics
dc.subject	HATS
dc.subject	HDACS
dc.subject	Επιγενετική
dc.title	Systemic lupus erythematosus and epigenetics	en
heal.type	journalArticle
heal.classification	Science
heal.classification	Biology
heal.classification	Επιστήμες
heal.classification	Βιολογία
heal.classificationURI	http://zbw.eu/stw/descriptor/15685-2
heal.classificationURI	http://zbw.eu/stw/descriptor/15633-0
heal.classificationURI	N/A-Επιστήμες
heal.classificationURI	N/A-Βιολογία
heal.contributorName	Κόλλια, Παναγούλα	el
heal.language	en
heal.access	free
heal.publicationDate	2009
heal.bibliographicCitation	Regkli, A., Konstadinedes, P.I., Mallis, P., Matsis, K., Constadinides, I., et al. (2009). Systemic lupus erythematosus and epigenetics. "e-Journal of Science & Technology". [Online] 4(4): 75-87. Available from: http://e-jst.teiath.gr/	en
heal.abstract	Human systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease characterized by autoantibodies to nuclear components with subsequent complex formation and deposition in multiple organs. A combination of genetic and environmental factors is required for disease development1. Apoptotic defects and impaired removal of apoptotic cells contribute to an overload of autoantigens that become available to initiate an autoimmune response2. Epigenetic factors have significant effects on T-cell functions by modulating its DNA methylation pattern and in patients with active lupus happens gene-specific DNA methylation. Also IL-2 contribute in the pathogenesis by reason of IL-2 regulate the tolerance mechanisms such as the activation induced cell death (AICD) and the induction and maintenance of regulatory T-cells3. DNA hypomethylation in CD4+ T-cells causes several gene activations and molecule overexpressions that alters cellular function. Moreover, histone deacetylase inhibitors reverse the skewed expression of multiple genes involved in SLE2. 5-azacytidine and other demethylating agents could induce lupus-like autoimmunity in vitro and in vivo. SLE is a predominantly female disease that affects more the female than the male. The etiology of SLE remains incompletely understood, although a number of genetic and environmental factors have been implicated, that may alter epigenetic regulation of gene expression. Epigenetics refers to heritable chromatin-based mechanisms in the regulation of gene expression without changing the DNA sequence. These mechanisms include DNA methylation, histone modification, abnormalities in ERK pathway signaling, and IL-2 transcriptional irregularity may be the key players through changes on gene expression in the development of this autoimmune disorder.	en
heal.publisher	Νερατζής, Ηλίας	el
heal.publisher	Σιανούδης, Ιωάννης	el
heal.journalName	e-Journal of Science & Technology	en
heal.journalName	e-Περιοδικό Επιστήμης & Τεχνολογίας	el
heal.journalType	peer-reviewed
heal.fullTextAvailability	true