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

Copyright © 2017 Elsevier Inc. All rights reserved.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 181(2017) vom: 15. Aug., Seite 51-59
Auteur principal: Brandt, D (Auteur)
Autres auteurs: Sergon, M, Abraham, S, Mäbert, K, Hedrich, C M
Format: Article en ligne
Langue:English
Publié: 2017
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Research Support, Non-U.S. Gov't Double negative T cells Effector memory T cells IFN-γ PD-1 Programmed death-1 Psoriasis CCR7 protein, human CD3 Complex plus... CD4 Antigens CD8 Antigens PDCD1 protein, human Programmed Cell Death 1 Receptor Receptors, Antigen, T-Cell Receptors, CCR7 Interferon-gamma 82115-62-6 Leukocyte Common Antigens EC 3.1.3.48
Description
Résumé:Copyright © 2017 Elsevier Inc. All rights reserved.
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
Description:Date Completed 28.08.2017
Date Revised 09.04.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2017.06.002