In this study we analyzed the immunological pathways involved at both systemic and peripheral levels, evaluating the correlations with clinical improvement. The objective of the study was to investigate the impact of functional blockade of TNF and IL-12 and IL-23 on the activity ofT lymphocytes in peripheral blood, with a focus on subpopulations that produce pro-inflammatory cytokines potentially involved in the pathogenesis of the disease and the immune response to antigens derived from pathogens like bacteria (Staphylococcus). In parallel, we assessed the modulation of gene expression in psoriatic plaque in correlation with clinical response to the treatment with two different classes of therapeutic agents—TNF and IL-12 and IL-23 antagonists. In the cohort of psoriasis patients, a significant increase in the level of expression of mRNA for IL-17 (p = 0.013) and IFN-c (p = 0.027) was seen in psoriatic plaques compared to the skin of healthy subjects. In patients treated with TNF-blockade, there was a statistically significant increase in the production of IL-10 (p = 0.006), IL-2 (p = 0.013), IL-17 (p = 0.013) and IFNc (p = 0.027) (Fig. 1) in PBMCs stimulated with anti-CD3. A previous study has already demonstrated a statistically significant linear correlation (p = 0.003) between the increase of IL-10 and PASI decrease in anti-TNF-treated patients, and no correlation between the increase in the secretion of other cytokines (IL-2, IL-17 and IFN-c) and clinical response to the treatment.
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