Abstract

Ultraviolet (UV) light generates damage to DNA which is removed by a versatile mechanism called nucleotide excision repair (NER). There are two subpathways for NER: the transcription coupled repair (TCR) pathway which removes DNA damage from actively transcribed genes and the global genome repair pathway which removes damage throughout the genome. Most types of DNA lesions are processed more rapidly by TCR than by GGR. It is widely accepted that immunological processes play a pivotal role in the generation of skin tumours induced by exposure to ultraviolet light and first evidence is emerging that GGR and TCR play different roles in skin reactions such as erythema and delayed type hypersensitivity. The relationship between UV-induced responses of the skin and the two NER subpathways is discussed.

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