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TCR+ CD3+ CD4− CD8− effector T cells in psoriasis

Abstract The autoimmune/inflammatory disorder psoriasis is characterized by keratinocyte proliferation and immune cell infiltration of the skin. TCR+ CD3+ CD4− CD8− “double negative” (DN) T cells can derive from CD8+ T cells through the down-regulation of CD8. The inhibitory molecule programmed deat...

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Bibliographic Details
Published in:Clinical immunology (Orlando, Fla.) Fla.), 2017-08, Vol.181, p.51-59
Main Authors: Brandt, D, Sergon, M, Abraham, S, Mäbert, K, Hedrich, C.M
Format: Article
Language:English
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Summary:Abstract The autoimmune/inflammatory disorder psoriasis is characterized by keratinocyte proliferation and immune cell infiltration of the skin. TCR+ CD3+ CD4− CD8− “double negative” (DN) T cells can derive from CD8+ T cells through the down-regulation of CD8. The inhibitory molecule programmed death (PD-)1 is expressed on activated T cells and plays a role in the maintenance of peripheral tolerance. A subset of DN T cells, characterized by the expression of PD-1, has recently been demonstrated to be self-reactive. We demonstrate that a majority of DN T cells exhibits effector memory phenotypes, express IFN-γ, and fail to proliferate. DN T cells from psoriasis patients are characterized by reduced DNA methylation of the IFNG gene and increased PD-1 expression. Furthermore, PD-1 positive DN T cells infiltrate the epidermis in psoriatic skin lesions. Our observations offer additional insight into the molecular pathophysiology of plaque psoriasis and show promise as potential disease biomarkers and/or therapeutic targets for future interventions.
ISSN:1521-6616
1521-7035
DOI:10.1016/j.clim.2017.06.002