Toll-like receptor 2 and type 2 diabetes.

Zahra Sepehri,Ali Akbar Nasiri,Zohre Kiani,Farhad Kohan

doi:10.1186/s11658-016-0002-4

Abstract

Innate immunity plays a crucial role in the pathogenesis of type 2 diabetes and related complications. Since the toll-like receptors (TLRs) are central to innate immunity, it appears that they are important participants in the development and pathogenesis of the disease. Previous investigations demonstrated that TLR2 homodimers and TLR2 heterodimers with TLR1 or TLR6 activate innate immunity upon recognition of damage-associated molecular patterns (DAMPs). Several DAMPs are released during type 2 diabetes, so it may be hypothesized that TLR2 is significantly involved in its progression. Here, we review recent data on the important roles and status of TLR2 in type 2 diabetes and related complications.

Highlights

Type 2 diabetes, referred to as adult-onset diabetes or as non-insulin-dependent diabetes mellitus (NIDDM) is increasingly common [1, 2]
The altered expression and functions of Toll-like receptor 2 (TLR2) and its intracellular molecular signaling may be associated with the mechanisms that result in the progression and pathogenesis of type 2 diabetes and its related complications
Another study identified that free fatty acids and high glucose levels upregulate the expression of TLR2 and TLR6, which resulted in increased activity of monocytes and increased production of superoxides, which are released in an nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB)-dependent manner [63]

Summary

Introduction

Type 2 diabetes, referred to as adult-onset diabetes or as non-insulin-dependent diabetes mellitus (NIDDM) is increasingly common [1, 2]. Elevated serum levels of innate immunity inflammatory cytokines such as IL-6 [19], IL-18 [20] and TNF-α [19] have been reported for subjects with type 2 diabetes and related complications. Toll-like receptor 2 (TLR2) plays significant roles in the induction of innate immune cells through a MYD88-dependent pathway [28, 29].

Results

Conclusion