C3D,G DEPOSITS IN INFLAMMATORY SKIN DISEASES - USE OF PSORIATIC SKIN AS A MODEL OF CUTANEOUS INFLAMMATION

Recent studies in our laboratories have shown that human keratinocytes synthesize and secrete complement components including C3. Moreover, human keratinocyte-derived C3 is regarded as a potential source of C3d ,g, a recently described constituent of the sublamina densa region of normal epidermal basement membrane. Additionally, human keratinocyte-d erived C3 may also contribute to epidermal basement membrane deposits of C3 in autoimmune or inflammatory skin disorders. To further our und erstanding of the specificity and origin of epidermal basement membran e C3 deposits in normal and diseased skin, we have characterized in si tu deposits of C3 and C3 cleavage fragments in various inflammatory sk in diseases and utilized a skin equivalent model to assess the deposit ion of C3 cleavage fragments in neo-basement membrane of epidermal out growths from normal or diseased human skin. C3d,g reactivity was found to be greater in all samples of inflamed skin, and typically associat ed with C3c reactivity at these sites. No immunoglobulins or other com plement components were detected. When lesional psoriatic skin rich in epidermal basement membrane C3c was used in our organ culture system, C3 incorporation within neo-basement membrane was observed. These res ults show that human keratinocyte-derived C3 may contribute to inflamm atory reactions in skin as well as account for deposits of C3d,g in no rmal epidermal basement membrane.