Vitiligo is an acquired and polygenic skin depigmenting disease characterized by bilateral, symmetrical depigmented patches over the entire body.~Its pathogenesis is multifactorial; however, the exact mechanisms that integrate the individual genetic susceptibility, melanocyte auto aggression, and failure of immune tolerance mechanisms are still not fully understood. The presence of these autoreactive CD8+ and CD4+ T cells in vitiligo patients' skin and blood samples . indicates a dysregulation of regulatory T-cell mechanism, which can suppress these cells.~Previous studies have reported an altered Treg cell frequency and function in vitiligo patients.~FoxP3 is the key transcriptional regulators of Tregs which mediate Treg cell function by repressing the expression of cytokines (IL2 and IL4 ) and upregulate the Treg cell markers (CTLA-4 and CD25 ).~Expression of IL-2 and its receptor CD25 are the most fundamental events in the host immune response. Thus any disorder in which T lymphocyte activation occurs at a substantial level is expected to induce expression of CD25 beyond ambient levels; this had been reported in atopic asthma, multiple sclerosis, allergic responses.~CD4+ CD25 FoxP3+ Tregs are important in maintaining self-tolerance and regulating immune responses in both physiological and pathological conditions .~Chemokines are important inflammatory factors that participate in many autoimmune responses.~C-X-C motif chemokine ligand 9 (CXCL9) is linked to the Th1 pattern and has been suggested as one of the most relevant chemokine axes that promote T-cell migration in different autoimmune and inflammatory processes.~In vitiligo, CXCL9 has been suggested to promote melanocyte-specic CTLs to in ltrate into the basal layer of the epidermis to attack melanocytes, resulting in the deficiency of melanin.
Clinical significance of circulating T regulatory cells , soluble CD25 and CXCL9 to assess disease activity of vitiligo.