Abstract
Several studies have determined the correlation between programmed cell death protein-1 (PD-1) and chronic plaque psoriasis (CPP). However, limited studies have assessed the association between PD-1 expression and the clinicoprognostic and distinct clinicopathological characteristics of CPP and guttate psoriasis (GP). Twenty-nine patients with skin biopsy-confirmed CPP were recruited at the Asan Medical Center between January 2018 and June 2020, and 33 patients with biopsy-confirmed GP were enrolled between January 2002 and June 2020. The clinicoprognostic and histopathological characteristics were analyzed according to immunohistochemical PD-1 expression in the epidermal or dermal inflammatory infiltrates. The CPP and GP lesions were divided into PD-1-low and PD-1-high groups. The CPP epidermal PD-1-high group had typical histopathological changes and significantly higher psoriasis area and severity index scores (p = 0.014) and disease duration (p = 0.009) than the epidermal PD-1-low group. In patients with GP, compared with the dermal PD-1-high group, the dermal PD-1-low group exhibited significantly higher disease duration (p = 0.002) and relapse rate of plaque psoriasis (p = 0.005) and significantly lower relapse-free survival (p = 0.016). Upregulated epidermal PD-1 expression was correlated with the chronicity and severity of CPP, while downregulated dermal PD-1 expression was correlated with poor prognosis of GP.
Highlights
Psoriasis is a chronic, recurrent inflammatory disease associated with the activation ofT cells, including T helper 17 (Th17) and Th1 cells, which promote cutaneous inflammation and keratinocyte hyperproliferation [1]
In addition to the immune-suppressing cytokines released from Treg cells, some T cell surface molecules, including cytotoxic T lymphocyte-associated antigen 4 (CTLA4), neurophilin-1, human leukocyte antigen G, and the programmed cell death protein-1 (PD-1) that interacts with the programmed cell death ligand (PD-L1), play critical roles in immune tolerance [3]
The mean age of 29 patients (21 men and 8 women) with chronic plaque psoriasis (CPP) was 46.00 years. Of these 29 patients, (48.3%) and (51.7%) patients were assigned to the epidermal PD-1-low (Figure 1A) and epidermal PD-1-high groups (Figure 1B), respectively
Summary
Recurrent inflammatory disease associated with the activation ofT cells, including T helper 17 (Th17) and Th1 cells, which promote cutaneous inflammation and keratinocyte hyperproliferation [1]. The pathogenesis of psoriasis is mediated by pro-inflammatory cytokines, including IL6, TNF-α, and IL1. Dysfunctional regulatory T (Treg) cells disrupt immune tolerance, which leads to the induction of autoimmune and auto-inflammatory diseases, such as psoriasis [2]. Dysfunctional T cell surface molecules cannot inhibit the activity of inflammatory cells in patients with psoriasis. PD-1, a glycoprotein expressed on the surface of various immune cells, including T cells, B cells, macrophages, and monocytes, binds to PD-L1 and PD-1LG2 and inhibits the function of effector T cells and promotes Treg cell activity [4]. PD-1 deficiency induces psoriasiform dermatitis, promotes the recruitment of activated cytotoxic CD8+ T cells in the epidermis, and upregulates the production of IL6 [6]. Recombinant PD-1 treatment alleviated psoriatic inflammation in a murine model of imiquimod-induced psoriasis [7]
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