## 4 Discussion
\begin{table}
\begin{tabular}{c c c} \hline \hline  & **Plaque Psoriasis** & **Plaque Psoriasis** & **Arthropathic** \\ **Psoriasis** & **versus Arthropathic** \\ **Psoriasis** (_p-Value_) & **Psoriasis** (_p-Value_) & **Psoriasis** (_p-Value_) \\ \hline GA + AA/GG & 0.5972 & 0.5116 & 0.3375 \\ \hline GA + GG/AA & 0.0009 & 0.1069 & 0.4028 \\ \hline CC + CT/TT & 0.3808 & 0.2960 & 0.4669 \\ \hline CT + TT/CC & 0.2817 & 0.0648 & 0.0280 \\ \hline \hline \end{tabular}
\end{table} 
Table 9: Statistical analyses according to models of inheritance. genetic links between psoriasis and various comorbidities that were based on immunogenic changes in different genes, alleles and loci [25]. Recent strides in technology and comprehensive GWAS studies have provided substantial proof of connections between psoriasis and numerous genes situated both within and outside the MHC [26]. Psoriasis is influenced by a complex interaction between genetic loci and environmental factors. Over 40 SNPs related to psoriasis have been identified through GWAS and targeted approaches, many of which are close to genes linked to adaptive and innate immunity pathways. The MHC class I, especially the _HLA-C*06:02_ allele, is the main genetic factor contributing to susceptibility to psoriasis. Various other genes associated with innate immunity and signaling pathways were also involved [27]. SNPs that affect processes such as skin barrier functions (Late Cornified Envelope 3E (LCE3E) and Late Cornified Envelope 3C (LCE3C)), IL-23 signaling (IL-23A, IL-23R, and IL-23) nuclear factor-kB and interferon signaling (Nuclear Factor Of Kappa Light Polypeptide Gene Enhancer In B-Cells Inhibitor, Alpha (_NFKBIA_), Long Intergenic Non-Protein Coding RNA 1185 (_LINC01185_), Tyrosine Kinase 2 (_TYK2_), Potassium Voltage-Gated Channel Subfamily H Member 7 (_KCNH7_), IL-28 RA, Tumor Necrosis Factor Alpha-Induced Protein 3 (_TNFAIP3_), Annexin A6 (ANXA6)) and IL-17 cell response (REV3 Like, DNA Directed Polymerase Zeta Catalytic Subunit ((_REV3L_), _TYK2, IL-23R_) were correlated with psoriasis risk [28; 29]. In our study, we analyzed the link between _PDCD1_ (rs10204525), _COL91A_ (rs550675) gene polymorphisms and psoriasis from an Eastern European population to bring new information into the complex genetic picture of this disease. The _PDCD1_ gene is mapped to 2q.37.3 and encodes a transmembrane glycoprotein (PD-1) which is a receptor with immune-inhibitory properties that gets expressed in activated T cells and participates in the control of T-cell functions, particularly those of effector CD8+ T cells. Additionally, it can facilitate the transformation of CD4+ T cells into T regulatory cells. _PDCD1's_ presence extends to numerous tumor types, including melanomas, and it has been established to exert an influence on antitumor immune responses. Furthermore, this protein has demonstrated its involvement in preventing autoimmune reactions [15]. The effect on the immune response of PD-1 is achieved by its ligands (PDL-1 and PDL-2), the former being expressed on various hematopoietic cells, non-hematopoietic cells but also non-immune cells such as endothelial cells, stromal cells, epithelial cells and keratinocytes [30]. A study of 10 psoriatic patients who were biopsied from skin lesions and immunohistochemistry analyzed with specific anti-PD-1 antibodies was performed. The results showed that PD-1 levels increased with inflammation in psoriatic plaques. Also, in this study, PD-1 was determined in experimental mice induced by applying miquimod 62.5 topically in 5%. Thus, elevated levels of PD-1 compared to the healthy sample were detected in samples collected from regional lymph nodes draining psoriatic skin, and when monoclonal antibody neutralizing against PD-1 was administered, mice with psoriasis showed exacerbation of lesions [31]. An article published by [PERSON] et al. in 2017 presented 5 patients with malignant tumor pathologies, 4 of whom had skin psoriasis lesions and one had a close family history of psoriasis.