<i>Psoralea corylifolia</i> L., (<i>P. corylifolia</i>), which is used for treating vitiligo in clinic, shows inhibitory and activating effects on tyrosinase, a rate-limiting enzyme of melanogenesis.
'TC' haplotype containing minor alleles of NPY polymorphisms was significantly higher in patients and increased the risk of vitiligo by 2.3 fold (p<0.0001).
(3) We replicated a previous association of FOXP3, a transcription factor that regulates T-cell development and function, with vitiligo; and (4) we discovered that C1GALT1C1 exhibits sex-specific effect on disease risk in both IBDs.
(3) We replicated a previous association of FOXP3, a transcription factor that regulates T-cell development and function, with vitiligo; and (4) we discovered that C1GALT1C1 exhibits sex-specific effect on disease risk in both IBDs.
(4) Conclusions: It remains unclear whether the <i>HLA-G</i> variants associated with vitiligo were detected because of the high linkage disequilibrium (LD) with HLA-A*02, or if the <i>HLA-A</i> variants previously reported as associated with vitiligo were detected because of the high LD with HLA-G*01:01:01:01/UTR-1, or if both genes jointly contribute to vitiligo susceptibility.
(4) Conclusions: It remains unclear whether the <i>HLA-G</i> variants associated with vitiligo were detected because of the high linkage disequilibrium (LD) with HLA-A*02, or if the <i>HLA-A</i> variants previously reported as associated with vitiligo were detected because of the high LD with HLA-G*01:01:01:01/UTR-1, or if both genes jointly contribute to vitiligo susceptibility.
125 Sudanese patients suffering from vitiligo were investigated for the distribution of serum proteins (haptoglobins and transferrins), red cell enzymes (acid phosphatase, 6-phosphogluconate dehydrogenase, phosphoglucomutase and glucose-6-phosphate dehydrogenase) and hemoglobins.
Vitiligo was significantly associated with single-nucleotide polymorphisms (SNPs) in a 30-kb LD block on chromosome 6q27, in close vicinity to IDDM8, a linkage and association signal for type I diabetes mellitus and rheumatoid arthritis.
Vitiligo risk associated with the MHC class I region thus derives from combined quantitative and qualitative phenomena: a SNP haplotype in a transcriptional regulator that induces gain-of-function, elevating expression of HLA-A RNA in vivo, in strong linkage disequilibrium with an HLA-A allele that confers *02:01 specificity.