6 research outputs found

    Frequency of <i>KIR</i> genotype profiles in patients with Vogt-Koyanagi-Harada (VKH) disease and healthy controls.

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    <p>Nineteen <i>KIR</i> genotypes were observed that differ from each other by the presence (indicated by grey shading) of 12 variable <i>KIR</i> genes. Genotypes for the centromeric and telomeric parts of the <i>KIR</i> locus were assigned according to the presence or absence of <i>A</i> and <i>B</i> haplotype defining <i>KIR</i> genes. Frame work genes (<i>3DL3</i>, <i>3DP1</i>, <i>2DL4</i>, <i>3DL2</i>) and pseudogene (<i>2DP1</i>) that were observed in all 405 studied subjects are not shown. The frequency of each genotype is presented in percentage frequency (%F) and defined as the number of individuals carrying the genotype (N) divided by the number of individuals studied (n) in the given study group. Significant difference between controls and patients was observed only in the distribution of genotypes with <i>AA-AA</i> (p = 0.007) or <i>AB-AA</i> (p = 0.05) constellations.</p

    <i>KIR-HLA</i> genotypes predictive of reduced NK cell education and response are associated with VKH.

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    <p>45.4% of VKH group lack the following 4 KIR/HLA factors: 3DL1+Bw4, 2DL2+C1/C2, 2DS2 and 2DS3, while only 30.6% of the controls display this genotypes (p = 0.002, OR = 1.9 [95% CI 1.28–2.83]).</p

    Human Embryonic Stem Cell-Derived Mesenchymal Stromal Cells Decrease the Development of Severe Experimental Autoimmune Uveitis in B10.RIII Mice

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    <p><i>Purpose</i>: We investigated the effect of exogenously administered human embryonic stem cell-derived mesenchymal stromal cells (hESC-MSCs) in experimental autoimmune uveitis (EAU) in B10.RIII mice, a murine model of severe uveitis.</p> <p><i>Methods</i>: B10.RIII mice were immunized with an uveitogenic peptide, and intraperitoneal injections of 5 million hESC-MSCs per animal were given on the same day. Behavioral light sensitivity assays, histological evaluation, cytokine production, and regulatory T cells were analyzed at the peak of the disease.</p> <p><i>Results</i>: Histological and behavioral evidence demonstrated that early systemic treatment with hESC-MSCs decreases the development of severe EAU in B10.RIII mice. hESC-MSCs suppress Th17 and upregulate Th1 and Th2 responses as well as IL-2 and GM-CSF in splenocytes from hESC-MSC-treated mice.</p> <p><i>Conclusions</i>: MSCs that originate from hESC decrease the development of severe EAU in B10.RIII mice, likely through systemic immune modulation. Further investigation is needed to determine any potential effect on active EAU.</p
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