Mast Cells Are a Marked Source for Complement C3 Products That Associate with Increased CD11b-Positive Cells in Keratinocyte Skin Carcinomas.

By using immunohistochemistry and antibodies that identify complement C3c (in C3 and C3b) or CD11b receptor, we report that the proportion C3c mast cells and the number of CD11b cells are increased in basal cell carcinoma (BCC). Instead, only CD11b cells are increased in squamous cell carcinoma/Bowen's disease, and only slightly so in actinic keratosis. Only C3c mast cells are increased in psoriasis.

Complement C3 is expressed by mast cells in cutaneous vasculitis and is degraded by chymase.

The complement factor C3 and chymase released from tryptase(+), chymase(+) mast cells may be involved in the pathogenesis of cutaneous leukocytoclastic vasculitis. To study whether mast cells contain C3 in vasculitis and whether chymase interacts with C3, cryosections from vasculitis biopsies were double-stained histochemically for C3c in tryptase(+) mast cells, as well as for chymase and vessel wall C3c, or they were treated with 5 µg/ml rh-chymase for 24 h followed by immunofluorescence (IF) analysis of C3c, IgG, IgM and IgA. The effect of rh-chymase on purified human C3, C3a and IgG was studied using SDS-PAGE electrophoresis and LAD2 mast cell cultures.