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- W2963684304 abstract "Recurrence of hydatid cysts in cystectomy patients has dramatically remained a serious concern within the surgical community. Predisposing factors for recurrence of hydatid cysts remained to be identified. Toll-like receptor (TLR) plays a pivotal role in bridging between acquired and innate immunity in cystic echinococcosis (CE) infection. 117 CE patients including 66 acute hydatidosis (AH; primary infection) and 51 recurrent hydatidosis (RH; chronic infection), and 117 ethnically matched healthy control (HC) were investigated from endemic regions of Iran in the period of 2015-2018. CE patients were definitely confirmed using histopathological and immunological assays. Genotyping of TLR2 Arg753Gln was carried out by restriction fragment length polymorphism and sequencing. The homozygous mutant-type TLR2 Gln/Gln (A/A) was represented to be associated with the occurrence of RH (P = 0.04) and conferred a 9 fold risk for susceptibility, while the heterozygous mutant-type TLR2 Arg/Gln (G/A) indicated a tendency to be associated with the occurrence of RH (P = 0.07). There was no discrepancy in the frequency of TLR2 Arg753Gln haplotypes between AH patients and HC individuals (P = 0.09). The mutant allele A was observed to be a risk factor for susceptibility to RH patients. Our results point to a clinical association between TLR2 Arg753Gln haplotypes with RH in postoperative patients. It can be inferred that allele G may lead to protection against the CE, while mutant allele A may be a diagnostic hallmark in the screening of RH susceptibility. Nevertheless, further studies with a larger sample size of different ethnic populations are required to authenticate this association." @default.
- W2963684304 created "2019-07-30" @default.
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- W2963684304 date "2019-10-01" @default.
- W2963684304 modified "2023-10-10" @default.
- W2963684304 title "A clinical association between Toll-like receptor 2 Arg753Gln polymorphism with recurrent cystic echinococcosis in postsurgery patients: A case control study" @default.
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- W2963684304 doi "https://doi.org/10.1016/j.cimid.2019.101336" @default.
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