Publications by authors named "Victoria L Arandhara"

Article Synopsis
  • The study investigates the genetic variations in the SR-BI gene, which plays a role in hepatitis C virus (HCV) entry into cells, by analyzing six specific single nucleotide polymorphisms (SNPs) in individuals with a history of HCV infection.
  • Findings reveal that the rs5888 variant allele T is more common in individuals with advanced liver fibrosis and relates to lower SR-BI mRNA levels in liver tissue samples.
  • The research suggests that the rs5888 variant may serve as a genetic marker to identify patients at higher risk for severe disease due to its link to decreased SR-BI expression and increased fibrosis progression.
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FcγRIIB-deficient mice generated in 129 background (FcγRIIB(129)(-/-)) if back-crossed into C57BL/6 background exhibit a hyperactive phenotype and develop lethal lupus. Both in mice and humans, the Fcγr2b gene is located within a genomic interval on chromosome 1 associated with lupus susceptibility. In mice, the 129-derived haplotype of this interval, named Sle16, causes loss of self-tolerance in the context of the B6 genome, hampering the analysis of the specific contribution of FcγRIIB deficiency to the development of lupus in FcγRIIB(129)(-/-) mice.

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Fc receptors for IgG (FcgammaR) have been implicated in the development of arthritis. However, the precise contribution of the individual FcgammaR to joint pathology is unclear. In this study, the role of the different FcgammaR was assessed both in an active and in a passive mouse model of arthritis by analyzing disease development in double and triple knockout (KO) offspring from crosses of FcgammaRI KO, FcgammaRIII KO, FcgammaRI/III double KO, or FcR gamma-chain KO with the FcgammaRII KO on C57BL6 background, which is susceptible for collagen-induced arthritis (CIA).

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