Immunologic biomarkers to predict efficacy of biological and systemic therapies for psoriasis

Psoriasis is one of the most common systemic chronic immune-mediated inflammatory diseases. Current treatment strategies for psoriasis focus on relieving symptoms, improving quality of life, and preventing disease progression. In the absence of a positive effect from the initial therapy, the issue of using various biological or low molecular weight drugs that affect certain immune mechanisms underlying the pathogenesis of the disease is considered. Current therapeutic strategies aim to develop new drugs that would block effector cytokine signaling. To date, there are no reliable predictors to predict which patient will respond positively to a particular type of systemic therapy. The search for biomarkers involved in the pathogenesis of the disease and/or reflecting the mechanism of action of drugs can help in answering these questions. The presented article will consider predictive immunological biomarkers of the effectiveness of psoriasis treatment with biological drugs (TNF-α inhibitors, IL-17 inhibitors, IL-23 inhibitors, type 4 phosphodiesterase inhibitors), which can be cytokines, chemokines, adipokines, soluble forms of cell surface receptors, markers of immune activation. In our paper, we do not consider new therapeutic strategies in psoriasis targeting small molecules that target JAK-STAT signaling pathways (Janus kinase inhibitors, tyrosine kinase 2 inhibitors, retinoid orphan nuclear receptor γt) preventing signaling downstream of IL-23 and IL-6. Given that many molecular cell mechanisms of the immune response are involved in the pathogenesis of psoriasis, it seems promising to search for combinations of these markers and draw up appropriate models for predicting an effective response to therapy based on them.