期刊
JOURNAL OF IMMUNOLOGY
卷 195, 期 2, 页码 421-425出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1500448
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资金
- Uehara Foundation
- National Psoriasis Foundation translational grant
- National Cancer Institute Grant [CA164225]
- Advancing a Healthier Wisconsin Research and Education Program Fund
- Ann's Hope Foundation for Melanoma research funds
- National Institute of Arthritis and Musculoskeletal and Skin Diseases/National Institutes of Health Grant [1R01AR063091-01A1]
- Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Cancer Research Program [W81XWH-14-1-0587]
- Grants-in-Aid for Scientific Research [15K09796] Funding Source: KAKEN
Programmed cell death 1 (PD-1) is a key regulatory molecule that has been targeted in human cancers, including melanoma. In clinical testing, Abs against PD-1 have resulted in psoriasiform dermatitis (PsD). To determine whether PD-1 regulates PsD, we compared skin responses of PD-1-deficient (PD-1KO) mice and wild-type (WT) controls in an imiquimod (IMQ)-induced murine model of psoriasis. PD-1KO mice showed severe epidermal hyperplasia, greater neutrophilic infiltration, and higher expression of Th17 cytokines (versus WT mice). IMQ exposure increased PD-1 expression by skin gamma delta-low (GDL) T cells and enhanced expression of PD-L1 by keratinocytes. Three-fold increases in the percentage of IL-17A(+) GDL T cells were observed in skin cell suspensions derived from IMQ-treated PD-1KO mice (versus WT controls), suggesting that the lack of PD-1 has a functional effect not only on alpha beta T cells, but also on GDL T cells, and that PD-1 may play a regulatory role in PsD.
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