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In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol
Published on: December 30, 2016
Association between FOXP3 polymorphisms and vitiligo in a Han Chinese population
1Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Changlexi Road No. 127, Xi'an, Shaanxi, 710032, China.
Genetic variations in the FOXP3 gene are linked to an increased risk of developing vitiligo, an autoimmune skin depigmentation disorder. These FOXP3 gene polymorphisms may contribute to vitiligo pathogenesis by affecting regulatory T-cell function.
Area of Science:
- Genetics
- Immunology
- Dermatology
Background:
- Vitiligo is an autoimmune disorder causing melanocyte loss and skin depigmentation.
- Dysfunction of CD4(+)CD25(+) regulatory T-cells (Tregs) is implicated in vitiligo pathogenesis.
- FOXP3 gene polymorphisms have been associated with other autoimmune diseases, suggesting a potential role in vitiligo.
Purpose of the Study:
- To investigate the association between FOXP3 gene polymorphisms and the risk of developing vitiligo.
- To explore the potential role of FOXP3 gene variations in vitiligo susceptibility.
Main Methods:
- A case-control study involving 682 vitiligo patients and 682 healthy controls.
- Genotyping of three FOXP3 single nucleotide polymorphisms (SNPs): rs2232365, rs3761548, and rs5902434 using PCR-SSP.
- Analysis of genotype and allele frequencies to determine association with vitiligo risk.
Main Results:
- The rs2232365 GG and rs3761548 AA genotypes were significantly associated with increased vitiligo risk.
- Carrying 2-6 variant alleles of the studied FOXP3 SNPs increased vitiligo risk.
- Elevated risk was observed in specific subgroups: older age (>20 years), male sex, active vitiligo, nonsegmental vitiligo, and those with other autoimmune diseases.
Conclusions:
- FOXP3 gene polymorphisms are a contributing factor to vitiligo risk in the Han Chinese population.
- These findings suggest a mechanism involving FOXP3 and Treg dysfunction in vitiligo development.
- Further research may elucidate targeted therapeutic strategies based on genetic predispositions.
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