الفهرس 
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Abstract
Diabetes mellitus is a metabolic disease characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long term damage, dysfunction and failure of various organs, especially the eye, kidney, nerves and blood vessels.
Potential triggers for immunologically mediated destruction of the beta cell include viruses (eg. enterovirus, mumps, rubella and coxsackie virus B4).
The immune response to virus infection begins with the recognition of pathogen-associated molecular patterns (PAMPs) as ‗non-self‘ signatures. This recognition occurs through host pattern recognition receptors (PRRs), and triggers intracellular signaling events that induce innate immunity.
Of the PRRs, the most extensively studied are TLRs, which are type 1 transmembrane glycoproteins. Human homologs are known to comprise at least 11 members with different response triggers. TLR3 has been shown to recognize double-stranded RNA (dsRNA), a molecular signature of most viruses, and it is expressed at high levels in human and mouse pancreatic β-cells and in antigen-presenting dendritic cells, suggesting a potential role for this receptor in the infectious etiology of T1DM.
The aim of this study was to investigate TLR3 genetic polymorphism (rs5743313) and its relation to susceptibility of diabetes in addition to its relation to glycemic control among children with T1DM.
The study was conducted on 110 subjects attended to pediatric department of Menoufia University during the period from October 2019 till December 2020.