Features of cellular immunity in patients with psoriasis and psoriatic arthropathy

Objective — to determine the characteristics of the immune phenotype of peripheral lymphocytes, particularly T- and NK-cells, in patients with psoriasis (Ps) and psoriatic arthropathy (PsA), with a focus on the expression levels of CD314 and CD94, in order to identify potential markers of disease activity and immunophenotypic differences between the forms of the disease. Materials and methods. The study included 30 patients divided into two groups. Group 1: 18 patients with plaque Ps (PASI 12,1), group 2: 12 patients with PsA (DAS28 4,6). Additionally. 20 healthy donors served as the control group. A basic immunogram was performed, along with analysis of CD314 and CD94 expression on T-lymphocytes (CD3+) and NK-cells (CD3–56+) using flow cytometry. Blood samples were collected twice with a 21-day interval. Statistical analysis was performed using Statistica 10,0 software and the Mann—Whitney U test, with a significance level of p < 0.05. Results and discussion. Significant immunophenotypic differences were identified between patients with Ps and PsA. In PsA patients, a statistically significant decrease in CD19+ B lymphocytes was observed, along with increased expression of CD314 on NK-cells. At the same time, the level of the inhibitory receptor CD94 was significantly reduced on T-lymphocytes. In patients with plaque psoriasis, a moderate increase in CD3–56+314+ cells and a slight decrease in CD3+94+ expression were noted, indicating latent activation of cytotoxic mechanisms. These findings suggest a disruption in the balance between activating and inhibitory signals in the immune system in PsA, which may underlie the more aggressive course of the disease. T-cell exhaustion (reduced CD3+314+94+) and chronic activation of the NKG2D receptor may contribute to persistent inflammation. In target tissues — the skin and joints — overexpression of NKG2D ligands enhances infiltration, cytokine production, and tissue destruction. NKG2D functions not only as an activator of cytotoxic cells but also as a modulator of immune sensitivity involved in tolerance formation or exhaustion. This opens prospects for its use as a therapeutic target in the treatment of Ps and PsA. Conclusions. Patients with PsA exhibit more profound impairments in cellular immune response compared to those with plaque Ps. Decreased CD94 expression and B-cell deficiency in PsA patients indicate immunosuppressive dysregulation potentially associated with disease severity. The identified immunophenotypic differences support the inclusion of CD314/CD94 markers in an extended immunogram as potential prognostic biomarkers. Future research should focus on the functional activity of cytotoxic cells and cytokine profiling (IL-10, IFN-γ, TNF-α) to refine pathogenetic targets for targeted therapy.