ABSTRACT
The effect of PUVA treatment on normal human serum (NHS), on isolated PMN, or on C3-deficient guinea pigs and congenic (C3-competent) control animals was tested. At a concentration of 0.1 or 1 mM/l 8-MOP and UVA doses of 5-30 J/cm2, PUVA failed to induce any detectable C3-cleavage in NHS. Furthermore, when the complement (C) activation in NHS had been induced before or after PUVA treatment by various methods. PUVA did not modulate the extent of C3-cleavage. PUVA did not affect the viability of isolated PMN, nor did it induce a release of LDH or elastase. No differences between C3-deficient and C-competent guinea pig skin exposed to PUVA were observed in erythema or histologic responses. Immunohistologic examination of specimens from normal guinea pigs revealed C3b and C3d deposits on necrotic keratinocytes, findings restricted to the PUVA-treated areas. Necrosis of keratinocytes was present in skin specimens of C3-deficient animals from PUVA-treated sites to a similar extent. However, deposits of C3-related antigens were completely absent there. From these observations, we suggest that the induction of phototoxic erythema following PUVA treatment is independent of complement.
Subject(s)
Complement System Proteins/physiology , Erythema/chemically induced , PUVA Therapy , Photosensitivity Disorders/chemically induced , Animals , Blood/radiation effects , Complement C3/analysis , Female , Guinea Pigs , Humans , Neutrophils/radiation effects , Ultraviolet RaysABSTRACT
In cryostat sections from lesional skin of a patient with pemphigus, a typical pattern of IgG deposits was detected at the epidermal intercellular space. However, there were no deposits of complement (C) components. By the highly sensitive APAAP technique using monoclonal antibodies, it was demonstrated that the IgG deposits consisted exclusively of IgG4. IgG subclass analysis of serum autoantibodies against epidermal intercellular substance antigen revealed an identical subclass restriction to IgG4. The IgG4 portion of the serum IgG fraction was significantly increased. Since IgG4 is known to be a an almost ineffective activator of complement, the lack of deposits of C components is not surprising. Our ex vivo observations suggest that complement is not essential for the induction of pemphigus acantholysis.
