Background: Psoriasis is an autoimmune-related chronic inflammatory skin disorder. Psoriasis vulgaris (PV) is the most common form of psoriasis. T regulatory cells (Tregs) are typically considered inhibitors of autoimmune responses. FOXP3 is a master control transcription factor for development and function of Tregs. FOXP3 gene polymorphism changes FOXP3 protein function and quantity leading to Tregs dysfunction that subsequently may be related to PV pathogenesis. Objective: The objective of the present study was to evaluate the possible role of FOXP3 gene (rs3761548) polymorphism in PV pathogenesis. Materials and Methods: One hundred sixty subjects were included in the present study (80 PV patients and 80 well-matched healthy controls). All participants were evaluated by detailed history, general examination, dermatological examination, and psoriasis area and severity index (PASI) score. The detection of FOXP3 gene (rs3761548) polymorphism in patients and controls by PCR-restriction fragment length polymorphism technique was done. Results: There was statistically significant increase in CC genotype and C allele in patients compared to controls, whereas there were non-significant differences in AA and AC genotypes. However, there were non-significant associations between genotype distribution and each of age, sex, family history, PASI score, hair affection, nail affection, hypertension, diabetes mellitus, and body mass index. Conclusion: FOXP3 gene (rs3761548) polymorphism may increase susceptibility of PV and share in its pathogenesis as it leads to changes in FOXP3 protein function and quantity that subsequently affect T-regs functions. Further investigations for the role of other FOXP3 genes polymorphisms in psoriasis pathogenesis and their effects on the treatment response in psoriasis patients are strongly recommended.

Background: Acne vulgaris (AV) is an inflammatory disease of pilosebaceous follicles. It has multifactorial causes and is manifested as blackheads, papules, pustules, nodules, as well as cysts. The significantly greater serum hepcidin values among acne cases that do not develop post-acne scarring support its antifibrotic activities that were clarified by its capability of impeding transforming growth factor β1(TGF β1) induced Smad3 phosphorylation. Objective: The aim of the current work was to assess hepcidin gene polymorphism and plasma hepcidin level in acne vulgaris cases of varying severity with and without post-acne scaring. Patients and Methods: This case-control study included a total of 30 cases with AV with no post-acne scars, 30 cases with AV and post acne scar and 30 subjects of age and gender matched healthy controls, attending at