Activation of bullous pemphigoid antigen gene in mouse ear epidermis by ultraviolet radiation

Bullous pemphigoid (BP) is an autoimmune blistering disease and is a photoaggravated dermatosis, but the mechanism of the aggravation is still unknown. Since damage to DNA initiates transcription of some genes, we investigated in epidermis of mouse ears the relationship between DNA damage by ultraviolet (UV) radiation and BP antigen (BP-Ag) gene activation. For this, albino male mice were irradiated with 254 nm wavelength UV for a total dose of 500 J m-2. At fixed times (0.5, 2, 24, 48 and 72 h) post-UV irradiation, mouse ears were cut off, frozen and sectioned. In the sections, it was found that immunohistochemically detectable pyrimidine dimers were observed in nuclei of all epidermal cells at 0.5 h that were almost repaired by 72 h; a frequency of single strand breaks in DNA detected by in situ nick translation started to increase in nuclei of all epidermal cell layers at 0.5 h and the increase continued up to 24 h; mRNA for BP-Ag localized by non-radioactive in situ hybridization appeared in nuclei of basal cells at 0.5 h and in both nuclei and cytoplasm at 2 h; and immunoreactive BP-Ag started to increase in the basal cell cytoplasm and in the basement membrane zone at 2 h. BP-Ag started to accumulate in the basement membrane zone at 2 h. It is suggested that UV radiation increased BP-Ag synthesis through BP-Ag synthesis through BP-Ag gene activation and that this reaction is a factor which aggravates BP following UV irradiation in BP patients.