مشخصات پژوهش

Psoriasis is a chronic, immune-mediated skin disorder characterized by excessive keratinocyte proliferation, immune cell infiltration, and systemic inflammation. Central to its pathogenesis is the interleukin-23/inreleukin-17 (IL-23/IL-17) axis, which promotes T helper 17 (Th17) cell activation and secretion of proinflammatory cytokines such as IL-17 and IL-23. The interleukin-23 receptor (IL23R) gene, which encodes the IL-23 receptor, plays a crucial role in regulating this signaling pathway. Genetic variations in IL23R can modulate the receptor's expression and function, leading to variable immune responses and disease susceptibility (1, 5, 6). Several studies and meta-analyses have confirmed associations between IL23R polymorphisms (notably rs11209026 and rs7530511) and psoriasis susceptibility, particularly in European and Asian populations (1, 4, 7, 8). However, data from the Middle East and Iraq remain limited, and the functional link between these polymorphisms and circulating biomarkers of inflammation such as IL-17, IL-23, and matrix metalloproteinase-9 (MMP-9) has not been well-established