## 4 Discussion
All 5 patients received anti-PD1/PDL1 immunotherapy for antitumor therapeutic purposes and experienced exacerbation of psoriatic skin lesions or their onset [32]. Six polymorphisms of the _PDCD1_ gene coding the PD-1 protein were studied in a Chinese population of psoriasis patients, including 128 subjects. Genomic DNA was extracted from peripheral blood and PD1.6 (rs10204525) G allele was observed to increase the risk of psoriasis [12]. Another study determined Messenger Ribonucleic Acid (mRNA) for the _PDCD1_ gene in the peripheral blood of 72 psoriasis patients and 35 healthy subjects, showing that _PDCD1_ expression is significantly lower in psoriatic patients [33]. Many studies have demonstrated the protective role of PD-1 and its ligands in psoriatic patients, but polymorphisms of the gene encoding this glycoprotein have not yet been extensively studied. In our study, we determined the PD1.6 polymorphism (rs10204525) for the _PDCD1_ gene and observed a higher frequency of the GG genotype in patients compared to the control group but without statistical significance. Different genetic results could be due to population differences, but also the small batches on which studieshave been done for this gene, requiring a larger number of subjects. _COL9A1_ gene is located on chromosome 6q13 and encodes one of the three proteins of the type IX collagen chain, which is a component of the extracellular matrix [34]. This protein is predominantly found in hyaline cartilage and the vitreous body of the eye. The gene that encodes it is associated with osteoarthritis, epiphyseal dysplasia, and Stickler syndrome [35]. Collagen is the main component of the articular cartilage matrix, the collagen network having an important role in joint biomechanics [36]. Type II collagen is the main component of articular cartilage, but other types of collagens III, VI, IX, X, XI, XII and XIV also contribute to the formation of the mature matrix. The exact roles fulfilled by collagens IX and XI within this complex arrangement are not yet entirely elucidated. However, their significance is unmistakable, given that mutations found within the _COL9_ and _COL11_ genes result in chondodysplasia phenotypes characterized by the premature onset of osteoarthritis [37]. In our study, we found a significant association of rs550675 (C/T) variant located in _COL9A1_ with psoriasis, but without being specific to psoriatic arthritis, as we would have expected. However, this could be investigated in the future by following patients over a long period of time and correlated with the development of psoriatic arthritis throughout the disease. The role of gene coding for different types of collagens in psoriasis and psoriatic arthritis has been studied. In a review published in 2020, collagen genes with potential involvement in the pathogenesis of psoriasis and psoriatic arthritis were synthesized, listing gene coding for collagen types I, II, III, V, VI, VII, VIII, IX, X, XI and XVII [38]. rs12488457 (A/C, _COL6A5_), rs13081855 (G/T, _COL8A1_) were associated with a higher risk of psoriasis and arthropathic psoriasis, rs3812111 (_COL10A1_) was associated with psoriatic arthritis, and the G allele of rs2910164 (C/G, _MIR146A_) showed high susceptibility to both diseases in a study published by [PERSON] et al. [39]. The study of epigenetic modification represents a revolutionary perspective for the targeted treatment. Epigenetic changes in _COL9A1_ have been studied in osteoarthritis, and Lysine-Specific Demethylase-1 (LSD1) is responsible for the negative regulation of the _COL9A1_ gene by specific chromatin marks in each promoter. The treatment with 5-azadeoxycylidine prevented the hypermethylation of the _COL9A1_ promoter associated with negative gene regulation [40; 41; 42]. Studies have been conducted on the regulation of PD-1 expression after various immune stimulation, but epigenetic changes in the coding gene under the influence of drugs have not been widely studied.