Elnaz Asghari - Islamic Azad University,Karaj
Hamidreza Agha Keydarali Naghash - Karaj Branch, Islamic Azad University,Karaj,Iran
Parviz Shayan - Faculty of Veterinary Medicine, Tehran University,Tehran,Iran
Seyed Shapoor Reza Shojaei - Islamic Azad University,Karaj

Toll-like receptors (TLRs) are highly conservedtransmembrane protein receptors that mediate innateimmunity for hostTLR is a major arm of the innate immune system in sensing pathogen associatedmolecular patterns (PAMP’s) and activates the immune system to contain the infections. TLR/MyD88 signaling has been reportedas the key pathway in a non-specific antimicrobial responseagainst T. gondiiThere are currently 10known human TLRs, each of them contributing tospecific recognition of particular pathogen-associatedmolecular patterns.As one member of the TLRsfamily, TLR4 widely expresses on macrophages,monocytes,cardiomyocytes,airway epithelial,adipose tissue, skeletal muscle and vascular endothelialand smooth muscle cells.TLR4 plays a key role in theprocess of the innate immune response, and activatesthe inflammatory cell via the NF-κB pathway byinducing the expression of a variety of cytokines andother molecules crucial to immune responses.The glycosylphosphatidylinositol(GPI) of T. gondii was demonstrated to trigger TLR4 signalingPathways.In inflammatory monocytes, T. gondii infectioninduced the production of interferon (IFN)-β throughTLR4 and MyD88 signaling.The purpose of this investigation will the determinationof the distribution of genotypes at single nucleotidepolymorphism (SNP) of the toll-like receptor 4 (TLR4)in humans infected with Toxoplasma gondii and the identificationof genetic changes predisposing to infection. development.Considering the role of TLR molecules in the developmentof T. gondii infection, as well as TLR genetic changes, we will decideto describe in this report theprevalence rates of the genotypeand alleles at the TLR4896 A> G SNP (rs4986790 ) in women infected with T. gondii in IRAN and comparethem to the prevalence rates observed in women uninfected controls.

TLR4 ,SNP,GPI,Toxoplasma gondii