COMPLEMENT DEPOSITS IN EPIDERMAL-CELLS AFTER ULTRAVIOLET-B EXPOSURE

Ultraviolet B (UVB) radiation is known to induce formation of sunburn cells (SBC) in the epidermis. Since it was unknown whether this proces s might be accompanied by complement (C) activation, we analyzed C-dep osition in skin biopsies taken before and 24 h and 48 h after UVB expo sure (fourfold minimal erythema dose or fourfold minimal phototoxic do se) from 14 patients (5 receiving potentially photosensitizing drugs a nd 9 without such medication) by immunohistology. Local C-activation w as visualized by direct or indirect immunofluorescence staining with p olyclonal antibodies against C3b, C3d, C5, C9 and monoclonal antibodie s to C3b, C3d, C9 and neoantigens on the terminal complement complex ( TCC). Neutrophils were identified immunohistologically by antibodies t o polymorphonuclear elastase. All but one specimen taken before UVB ir radiation were completely negative; biopsies obtained 24 h after UVB r evealed complement C3b- and/or C3d-deposits within scattered cells of the epidermis, with wide individual variations in the number of C3-pos itive cells. C3b and TCC were found predominantly in the cytoplasma; C 3d deposits were more often accentuated at the cell surface of C-posit ive cells. A significantly higher number of keratinocytes was C3d-posi tive 48 h after UVB exposure than in specimens taken 24 h after UVB. S uch a reactivity pattern might indicate a rapid decay of intracellular C3b to C3d. Patients medicated with potentially photosensitizing drug s developed significantly higher numbers of strongly C3-positive cells than those without such medication. Infiltration with elastase-positi ve cells, presumably representing neutrophils, was observed in the upp er third of the dermis and the epidermis in all but one biopsy (n = 9) after UVB. As judged by phase contrast microscopy, nuclear structures were mainly absent in both C-positive cells and SBC. The good correla tion of C-positive epidermal cells with the number of eosinophilic SBC strongly suggested at least a partial identity of the cell population s. However, C3b- or C3d-positive keratinocytes were present in signifi cantly higher numbers than eosinophilic SBC detected by conventional h ematoxylin/eosin staining. Thus, C-activation might occur at an early step. The specificity of our staining results with polyclonal compleme nt antibodies was confirmed by monoclonal antibodies. Our findings ind icate that UVB irradiation consistently induces complement deposits in single epidermal cells distributed with an epidermal pattern identica l to that of SBC and that the complement system is activated, presumab ly via the alternative pathway. The results suggest that the complemen t-positive cells are identical with SBC and that epidermal complement activation might play an important role in the late phase of sunburn r eaction, especially in the UVB-mediated polymorphonuclear leukocyte in filtration of the skin.