Abstract
In vivo and in vitro animal experitnents have been performed to clarify the role of ultraviolet light denatured DNA (UV DNA) and ultraviolet light (UVL) in the pathogenesis of the dermal lesions of human SLE. Rabbits immunized with UV DNA show deposition of immunoglobulin at the dermal‐epidermal junction following exposure to UVL. We have also shown that UV DNA appears concomitantly with the antibody at the dermal‐epidermal junction subsequent to the UVL exposure. Both n DNA and UV DNA have been shown to bind to the dermal‐epidermal junction in vitro which could result in the persistence of these antigens at this site. These studies lend further support to the hypothesis that the release of UV DNA and its subsequent deposition at the dermal‐epidermal junction may result in binding of both immunoglobulin and complement, leading to the development of histological lesions of SLE.