Tregs CD25 CXCL9 in Vitiligo

CD25 Deficiency, Chemokine (C-X-C Motif), Tregs, Vitiligo

Clinical significance of circulating T regulatory cells , soluble CD25 and CXCL9 to assess disease activity of vitiligo.

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.

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