David Norris has proposed a four step model for the pathogenesis of LESSD (1): (1) exposure to UV light induces the release of proinflammaotry epidermal and dermal mediators such as IL-1 and TNF-alpha; (2) these mediators induce changes in epidermal and dermal cells including the induction of adhesion molecules and promotion of the translocation of normally intracellular autoantigen such as Ro/SS-A to the surface of epidermal cells; (3) autoantibody from the circulation binds to autoantigens such as Ro/SS-A that have been translocated to the surface of epidermal keratinocytes and (4) keratinocyte cytotoxicity ensues as the results of lymphoid cells that have been recruited from the circulation recognizing and responding to the Fc domains of autoantibody molecules bound to autoantigen expressed on the surface of keratinocytes (i.e.
C0040715
Chromosomal translocation