17 research outputs found

    Implementation of an Ultraviolet Phototherapy Service at a National Referral Hospital in Western Kenya: Reflections on Challenges and Lessons Learned

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    Evergon et Jean-Jacques Ringuette, Housebound: Portraits from the Winter Garden, Galerie Trois Points, Montréal. Du 11 mars au 29 avril 2017

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    <div><p>Background</p><p>The immunopathogenic mechanisms leading to psoriasis remain unresolved. CD57 is a marker of replicative inability and immunosenescence on CD8+ T cells and the proportion of CD57 expressing CD8+ T cells is increased in a number of inflammatory conditions.</p> <p>Methodology</p><p>We examined the expression of CD57 on T cells in the skin of patients affected with psoriasis, comparing lesional and unaffected skin. We also assessed functionality of the T cells by evaluating the secretion of several inflammatory cytokines (IL-17A, IFN-gamma, IL-2, IL-33, TNF-alpha, IL-21, IL-22, and IL-27), from cell-sorted purified CD4+ and CD8+ T cells isolated from lesional and unaffected skin biopsies of psoriasis patients.</p> <p>Principal Findings</p><p>We observed that the frequency of CD57+CD4+ and CD57+CD8+ T cells was significantly higher in unaffected skin of psoriasis patients compared to lesional skin. Sorted CD4+ T cells from psoriatic lesional skin produced higher levels of IL-17A, IL-22, and IFN-gamma compared to unaffected skin, while sorted CD8+ T cells from lesional skin produced higher levels of IL-17, IL-22, IFN-gamma, TNF-alpha, and IL-2 compared to unaffected skin.</p> <p>Conclusions/Significance</p><p>These findings suggest that T cells in unaffected skin from psoriasis patients exhibit a phenotype compatible with replicative inability. As they have a lower replicative capacity, CD57+ T cells are less frequent in lesional tissue due to the high cellular turnover.</p> </div

    Sorted CD4+ T cell cytokine production.

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    <p>Cytokine production by sorted CD4+ T cells from unaffected and lesional skin from psoriasis patients, with stimulation with PMA-ionomycin. Comparative chart representing IL-17A, IL-22, IL-2, IFN-gamma, TNF-alpha and IL-27. * = p<0.05.</p

    Association Testing of KIR3DS1 with Psoriasis.

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    <p>The combination of KIR3DS1 and HLA-B Bw4-80I has a large effect on psoriasis susceptibility, whereas KIR3DS1 without Bw4-80I, and Bw4-80I without KIR3DS1, have little effect. Thus, the compound genotype KIR3DS1+Bw4-80I drives the individual associations of KIR3DS1 and Bw4-80I with psoriasis (bottom two rows).</p>a<p>Frequencies of individuals positive for each allele.</p>b<p>p-values were tested by a two-sided Fisher's exact test (dominant model).</p>c<p>Logistic regression based conditional association testing of “KIR3DS1+Bw4-80I” on HLA-C*06:02 remained significant at p = 9.99×10<sup>−5</sup>, OR = 3.16 [1.77–5.63], whereas conditional testing of “Bw4-80I without KIR3DS1” on HLA-C*06:02 resulted in a non-significant p-value of 0.579, OR = 1.14 [0.72–1.80]. Thus, Bw4-80I does not have an independent effect on psoriasis susceptibility in the absence of KIR3DS1.</p

    Sorted CD8+ T cell cytokine production.

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    <p>Cytokine production by sorted CD8+ T cells from unaffected and lesional skin from psoriasis patients, with stimulation with PMA-ionomycin. Comparative chart representing IL-17A, IL-22, IL-2, IFN-gamma, TNF-alpha and IL-27. * = p<0.05, ** = p<0.01.</p
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