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1.
Dermatol Res Pract ; 2015: 145409, 2015.
Article in English | MEDLINE | ID: mdl-26788051

ABSTRACT

Background. Vitiligo is an acquired depigmentary skin disorder resulting from autoimmune destruction of melanocytes. Regulatory T cells (Tregs), specifically CD4(+)CD25(+) and Forkhead box P3(+) (FoxP3(+)) Tregs, acquired notable attention because of their role in a variety of autoimmune pathologies. Dysregulation of Tregs may be one of the factors that can break tolerance to melanocyte self-antigens and contribute to vitiligo pathogenesis. Methods. In order to sustain the role of Tregs in pathogenesis and disease activity of vitiligo, surface markers for CD4(+)CD25(+) and FoxP3(+) peripheral Tregs were evaluated by flow cytometry in 80 Egyptian patients with nonsegmental vitiligo in addition to 60 healthy control subjects and correlated with clinical findings. Results. Vitiligo patients had significantly decreased numbers of both peripheral CD4(+)CD25(+) and FoxP3(+) T cells compared to control subjects (11.49% ± 8.58% of CD4(+) T cells versus 21.20% ± 3.08%, and 1.09% ± 0.96% versus 1.44% ± 0.24%, resp., P < 0.05 for both). Peripheral numbers of CD4(+)CD25(+) and FoxP3(+) Tregs correlated negatively with VIDA score. Conclusion. Treg depletion with impaired immune downregulatory function might play a key role in the autoimmune conditions beyond nonsegmental vitiligo particularly in active cases. Effective Treg cell-based immunotherapies might be a future hope for patients with progressive vitiligo.

2.
Indian J Hematol Blood Transfus ; 25(2): 70-7, 2009 Jun.
Article in English | MEDLINE | ID: mdl-23100979

ABSTRACT

Iron deficiency anemia (IDA) is one of the most prevalent micronutrient deficiencies particularly in the developing countries. While there is evidence of an altered immune profile in iron deficiency, the exact immunoregulatory role of iron is not known. Knowledge particularly in children, who are vulnerable to iron deficiency and infection, is lacking. We aimed to study the effects of IDA and its treatment with oral iron supplementation on cell-mediated immunity. The levels of T-lymphocytes, their CD4(+), CD8(+) and CD1a(+) subsets, transferrin receptor (CD71) and serum ferritin were evaluated in 40 iron-deficient and 40 healthy children. The impact of oral iron supplementation for three months on the same parameters was also noted in children with IDA. The level of mature T-lymphocytes (CD4(+) and CD8(+)) was significantly lower (P<0.001) while that of the immature T-cells (CD1a(+)) was significantly higher (p<0.001) in IDA children compared to the control. The mature T-cell count was significantly improved after iron therapy. In spite of significant reduction in the immature T-cells (CD1a(+)) level after iron supplementation, it was significantly higher than the control. The present study demonstrated that T-lymphocytes maturation was defective in IDA and improved partially after 3 months of iron supplementation. Therefore, longer time of iron therapy may be required to induce complete maturation of T-lymphocytes.

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