کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3342455 1214287 2008 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Ubiquitination system and autoimmunity: The bridge towards the modulation of the immune response
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Ubiquitination system and autoimmunity: The bridge towards the modulation of the immune response
چکیده انگلیسی

The ubiquitination system comprises a highly specific and regulated post-translational mechanism by which the immune response can be modulated, setting the balance between immunity and tolerance. Proteolysis dependent and independent mechanisms have been implicated. Particularly, the role of ubiquitin ligases as modulators of central and peripheral tolerance has brought attention to this system as one of the key elements of a complex regulatory network designed to maintain an active surveillance system. Cbl-b, GRAIL and Itch are the main E3 ligases, considered as negative regulators of the immune response as part of the genetic program induced by the calcium/calcineurin pathway. Other key signaling pathways for the immune response, such as the NF-κB and TGF-β signaling are prone to be modulated by these ubiquitin ligases. Diverse mechanisms have been implicated in the development of anergy associated to E3 ligases, among these, the setting for TCR responsiveness and repression of cytokine transcription are best well characterized. Also, a role as inductors of regulatory T cells has been evidenced for Cbl-b and GRAIL. The defective expression of some of these E3 ligases has been related to the development of autoimmune disease, in experimental murine and human models, remarking its possible pathogenic role.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Autoimmunity Reviews - Volume 7, Issue 4, February 2008, Pages 284–290
نویسندگان
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