Academic Journal

Type 2 diabetes mellitus - an autoimmune disease?

التفاصيل البيبلوغرافية
العنوان: Type 2 diabetes mellitus - an autoimmune disease?
المؤلفون: Velloso, L Augusto, Eizirik, Decio L., Cnop, Miriam
المصدر: Nature reviews. Endocrinology, 9 (750-755
سنة النشر: 2013
المجموعة: DI-fusion : dépôt institutionnel de l'Université libre de Bruxelles (ULB)
مصطلحات موضوعية: Sciences bio-médicales et agricoles
الوصف: Inflammation-induced inhibition of the insulin signalling pathway can lead to insulin resistance and contribute to the development of type 2 diabetes mellitus (T2DM). Obesity and insulin resistance are associated with a chronic but subclinical inflammatory process that impairs insulin action in most tissues and could also hamper pancreatic β-cell function. The involvement of monocytic cells and the profiles of the chemokines and cytokines induced by this inflammation suggest an innate immune response. However, emerging data indicate that elements of the adaptive immune system could also be involved. As activation of an adaptive response requires antigen specificity, some researchers have hypothesized that T2DM evolves from an innate immune response to an autoimmune condition. In this Perspectives article, we present the arguments for and against this hypothesis and discuss which mechanisms could be involved in a putative switch from innate immunity to autoimmunity. © 2013 Macmillan Publishers Limited. ; SCOPUS: re.j ; info:eu-repo/semantics/published
نوع الوثيقة: article in journal/newspaper
وصف الملف: 1 full-text file(s): application/pdf
اللغة: English
Relation: uri/info:doi/10.1038/nrendo.2013.131; uri/info:pii/NRENDO2013131; uri/info:pmid/23835371; uri/info:scp/84888203171; https://dipot.ulb.ac.be/dspace/bitstream/2013/146066/3/vellsso.pdf; http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/146066
الاتاحة: http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/146066
https://dipot.ulb.ac.be/dspace/bitstream/2013/146066/3/vellsso.pdf
رقم الانضمام: edsbas.3F272230
قاعدة البيانات: BASE