Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSPBATISTA, Mariana D.TINCATI, CamillaMILUSH, Jeffrey M.HO, Emily L.NDHLOVU, Lishomwa C.YORK, Vanessa A.KALLAS, Esper G.KALIL, JorgeKEATING, Sheila M.NORRIS, Philip J.CHANG, DavidUNEMORI, PatrickLESLIE, Kieron S.MAURER, TobyLIAO, WilsonNIXON, Douglas F.2013-09-232013-09-232013PLOS ONE, v.8, n.2, article ID e52144, 6p, 20131932-6203https://observatorio.fm.usp.br/handle/OPI/1763Background: 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. Methodology: 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. Principal Findings: 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. Conclusions/Significance: 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.engopenAccesshuman keratinocytesatopic-dermatitisgene-expressionil-22differentiationlymphocytesimmunopathogenesisactivationimmunitysubsetarticleCopyright PUBLIC LIBRARY SCIENCE10.1371/journal.pone.0052144Multidisciplinary Sciences