title: TLR3 and its roles in the pathogenesis of type 2 diabetes.
abstract: Type 2 diabetes (T2D) is the most prevalent non&mdash;infectious disease and leads to several complications including nephropathy and retinopathy. The mechanisms and signaling molecules responsible for the development and progression of T2D, as well as its associated complications are yet to be identified. It would appear that genetic backgrounds and immunological parameters of people susceptible to T2D may play important roles in induction of T2D. TLRs participate in several cellular pathways which can induce activation of proliferation. However, in contradiction, these pathways can also be associated with apoptosis. The multiple roles of TLRs and their signaling molecules associated with T2D pathways makes them candidates for the induction of immune&mdash;regulated diseases like T2D. TLR3 has been identified as an intracellular ligand and subsequently activates signaling molecules via the TRIF pathway. Therefore, the alteration of expression of TLR3 and their functions may lead to inappropriate induction of immune system functions that are related to T2D disease. The aim of this review was to collect recent data regarding the roles of TLR3 in the progression and pathogenesis of T2D.
authors.affiliation: Zabol University of Medical Sciences Department of Internal Medicine Zabol Iran.
authors.forename: Z
authors.initials: Z
authors.lastname: Sepehri
authors.affiliation: Kerman University of Medical Sciences Department of Medicine Kerman Iran.
authors.forename: Z
authors.initials: Z
authors.lastname: Kiani
authors.affiliation: Zabol University of Medical Sciences Zabol medicinal plant research center Zabol Iran.
authors.forename: F
authors.initials: F
authors.lastname: Javadian
authors.affiliation: Zabol University of Medical Sciences Department of Anesthesiology Zabol Iran.
authors.forename: A
authors.initials: A
authors.lastname: Akbar Nasiri
authors.affiliation: Zabol University of Medical Sciences General Physician Zabol Iran.
authors.forename: F
authors.initials: F
authors.lastname: Kohan
authors.affiliation: Zabol University of Medical Sciences General Physician Zabol Iran.
authors.forename: S
authors.initials: S
authors.lastname: Sepehrikia
authors.affiliation: Zabol University of Medical Sciences Department of Health Zabol Iran.
authors.forename: S
authors.initials: S
authors.lastname: Javan Siamardi
authors.affiliation: Zabol University of Medical Sciences Department of Internal Medicine Zabol Iran.
authors.forename: H
authors.initials: H
authors.lastname: Aali
authors.affiliation: Faculty of Medicine, Kerman University of Medical Sciences Department of Immunology Kerman Iran h.daneshvar&commat;bio.gla.ac.uk.
authors.forename: H
authors.initials: H
authors.lastname: Daneshvar
authors.affiliation: Griffith University School of Natural Sciences and Eskitis Institute for Drug Discovery Brisbane Australia.
authors.forename: D
authors.initials: D
authors.lastname: Kennedy
mesh_terms: D017209:Apoptosis; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D015398:Signal Transduction; D051196:Toll-Like Receptor 3 / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: C495344:TLR3 protein, human; D051196:Toll-Like Receptor 3