A functional single-nucleotide polymorphism in the ERCC1 gene alters the efficacy of narrowband ultraviolet B therapy in patients with active vitiligo in a Chinese population

Summary Background T lymphocytes have been shown to cause the destruction of melanocytes in vitiligo pathogenesis. Narrowband ultraviolet B (NB‐UVB), as an effective therapeutic strategy in vitiligo, can lead to the formation of DNA photoproducts such as cyclobutane pyrimidine dimers (CPDs) in perilesional lymphocytes and thus induce skin immunosuppression. The repair of DNA photoproducts is performed mainly through the nucleotide excision repair (NER) pathway. We hypothesized that single‐nucleotide polymorphisms (SNPs) in NER genes might influence the repair capacity of CPDs and thus contribute to variations in phototherapy efficiency. Objectives To detect genetic polymorphisms in NER genes and their relationship with the efficacy of NB‐UVB therapy in patients with active vitiligo. Methods We investigated the association of NER SNPs (XPA A23G, XPC Ci11A, XPC C2919A and ERCC1 C118T) with phototherapy efficacy in 86 patients with vitiligo who received NB‐UVB treatment. Furthermore, we examined the impact of ERCC1 C118T on the apoptosis of T lymphocytes and CPD accumulation after NB‐UVB irradiation. Results We found that patients with vitiligo with the ERCC1 codon 118 CC genotype showed better efficacy after NB‐UVB irradiation than those with the ERCC1 118 TT and CT genotypes, whereas no such association was documented among the genotypes of XPA A23G, XPC Ci11A or XPC C2919A. Additionally, the apoptosis rates and CPD levels of lymphocytes after NB‐UVB irradiation in patients with the ERCC1 118 CC genotype were significantly higher than those in patients with the ERCC1 118 TT and CT genotypes. Conclusions The ERCC1 118 CC genotype confers better efficacy of NB‐UVB therapy in patients with active vitiligo. What's already known about this topic? One of the therapeutic mechanisms of narrowband ultraviolet B (NB‐UVB) in vitiligo is through the induction of skin immunosuppression during irradiation, especially by the apoptosis of lymphocytes. The repair of DNA damage after NB‐UVB radiation is performed mainly through the nucleotide excision repair (NER) pathway. The ERCC1 gene encodes one of the core proteins in the NER pathway. What does this study add? The ERCC1 codon 118 CC genotype can lead to an increase of DNA photoproducts and induce the apoptosis of T lymphocytes under NB‐UVB irradiation. Individuals carrying the ERCC1 118 CC genotype can experience better efficacy of NB‐UVB therapy.