الفهرس | Only 14 pages are availabe for public view |
Abstract Vitiligo is an acquired pigmentary disorder of unknown etiology that is clinically characterized by the development of white macules related to the selective loss of melanocytes, affecting around 2% of world’s population. Clinically, there are two types of vitiligo, localized vitiligo which can be segmental or focal, and generalized vitiligo. The course of the disease is unpredictable. The exact pathophysiology of vitiligo is not fully understood and is likely multifactorial. Interleukin-32 (IL-32) is a comparatively newly discovered cytokine and studies on it are still in their early stages. Studies have shown that it is produced by various cell types including T lymphocytes, natural killer cells, monocytes, and epithelial cells. Of particular importance, IL-32 exhibits numerous classical proinflammatory activities. It stimulates the production of numerous cytokines including TNF-α, IL-1β, and IL-6. It also activates proinflammatory signaling pathways such as mitogen-activated protein kinase (MAPK)-p38, extracellular receptor kinases (ERK), and NF-kB. It has four isoform variants, IL-32α, IL-32β, IL-32γ, and IL-32δ.Among all IL32 isoforms, IL-32α is the most abundant cDNA clone and has major proinflammatory activity of IL-32. The proinflammatory role of IL-32 has been well reported in several disorders including rheumatoid arthritis, cancers, pulmonary tuberculosis, systematic lupus erythematosus, and also in many skin disorders such as atopic dermatitis, hidradenitis suppurativa, leishmaniasis, and psoriasis. However, the role of IL-32 in vitiligo was not evaluated till now. The aim of this study was to investigate the possible role of IL32 on pathogenesis of vitiligo and correlate the estimated results with the clinical aspects of vitiligo. Fifty patients with active non segmental vitiligo from both sex and any age and forty healthy volunteer controls were enrolled in the study. Patients with VIDA +1 or more were included in the trial. For all participants, full medical history, dermatological examination was performed. Also, CBC, HbA1c and lipid profile will be done for all cases and controls. IL32 isoforms (α and β) gene expression was measured by real time polymerase chain reaction (RT-PCR) while IL32 serum level was measured by enzyme linked immune sorbent assay (ELISA). |