## 3 Ways to Assess Psoriasis Severity and Therapeutic Strategies for Psoriasis Treatment
### New Therapeutic Approaches in the Treatment of Psoriasis
#### 3.3.2. Biologic Drugs as a New Era of Psoriasis Treatment  
To date, psoriasis treatment approaches, which include ultraviolet radiation therapy and topical drug therapy, have shown the greatest efficacy in patients with mild to moderate posoriasis [23; 34]. In moderate to severe cases, however, the efficacy of these therapeutic strategies may be limited. When used as monotherapy or as part of combination therapy, biologic drugs have high efficacy and a favorable safety profile, making them an important tool in the treatment of advanced forms of psoriasis [34; 37; 38]. The therapeutic success of biologic drugs, which are most often peptides, is due to their ability to mimic the function of human proteins. This allows them to modulate cellular receptor activity and intermolecular interactions [38]. Biological agents so far used in the treatment of moderate-to-severe plaque psoriasis include drugs with mechanisms of action based on inhibition of various inflammatory pathways, including tumor necrosis factor alpha (TNF-a), interleukins 17, 23 and 36 (IL-17, IL-23, IL-36), Janus kinase (JAK), nuclear receptors RORyt and protein kinase ROCK2 [27]. Interleukin-17 Inhibitors  
The most recent biologic drugs registered by the European Medicines Agency (EMA) that interact with the IL-17 ligand or its receptor include those listed in (Figure 2). The interleukin-17 (IL-17) family of cytokines, which includes the IL-17A-F isoforms, plays an important role in the intercellular signaling network that is responsible for maintaining local tissue homeostasis [39]. These cytokines are involved in the recruitment of neutrophils within psoriatic lesions, contributing to the inflammation associated with psoriasis [40]. The most recently registered and approved (Figure 2) biologic in the therapeutic area of psoriasis is bimekizumab. It is a humanized, monoclonal antibody of the IgG1 subclass [38] that binds to interleukins IL-17A, IL-17F and IL-17 AF, which are transmitter molecules responsible for the body's natural defense mechanisms [41; 42]. This combination prevents the interaction of the aforementioned cytokines with specific receptors, which reduces inflammation and alleviates disease symptoms. According to studies, the dual potent and selective neutralization of IL-17A and IL-17F shows greater efficacy compared to previously registered secukinumab [39; 42]. Bimekizumab has emerged as a new and promising form of therapy for psoriatic lesions [42]. Brodalumab has shown high therapeutic efficacy in patients for whom previous treatment with other IL-17 inhibitors has been ineffective [38]. Its unique mechanism of action involves blocking the IL-17 receptor and neutralizing IL-17A, IL-17F, IL-17A/F, IL-17C and  
Figure 2: Biologic drugs that act by inhibiting IL-17 [34; 37; 38; 41]. IL-17E isoforms, resulting in reduced pro-inflammatory activity and improved therapeutic outcomes [34; 37]. Brodalumab shows comparable antiposoriatic effects to ixekizumab, a slightly earlier registered IL-17 inhibitor [38]. Ixekizumab is a humanized IgG4 monoclonal antibody with high affinity for IL-17A and IL-17A/F [34; 37; 38]. It has been singled out by the Food and Drug Administration (FDA) as the only drug recommended for the treatment of genital psoriasis [34]. Guselkumab, risankizumab and tildrakizumab are the most recent and effective interleukin 23 (IL-23) inhibitors used in the treatment of psoriasis (Figure 3). Interleukin 23 plays a key role in the pathomechanism of psoriasis, primarily through the activation and maintenance of the Th17 lymphocyte population [38]. It stimulates the proliferation and survival of these cells, leading to the release of pro-inflammatory mediators, such as IL-17 and IL-22, which increase inflammation and promote keratinocyte proliferation [38; 40]. Risankizumab is a humanized IgG1 monoclonal antibody that selectively blocks IL-23 by binding to the p19 subunit [34; 37]. The drug, acting by inhibiting IL-23, suppresses IL-23-dependent intercellular signaling and the release of pro-inflammatory cytokines [43].