Abstract

Type 2 diabetes (T2D) is the most prevalent non—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—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.