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The use of antibody to C 5b−9 in the subclassification of lupus erythematosus
Author(s) -
MAGRO C.M.,
CROWSON A.N.,
HARRIST T.J.
Publication year - 1996
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.1996.117852.x
Subject(s) - anti nuclear antibody , medicine , antibody , pathology , vasculitis , lupus erythematosus , discoid lupus erythematosus , immunofluorescence , skin biopsy , monoclonal antibody , immunology , antigen , connective tissue disease , lupus anticoagulant , dermatology , biopsy , autoantibody , autoimmune disease , disease
Summary Fifty‐five patients with biopsy‐proven cutaneous lupus erythematosus (LE) were identified in whom a prospective and retrospective review of the clinical and laboratory data allowed subclassification into systemic (SLE). subacute (SCLE). or discold (DLE) variants. In addition to conventional direct immunofluorescence. an indirect immunolluorescent technique. using a monoclonal antibody, was employed to assess deposition of the membranolytic attack complex (C 5b−9 ) in skin lesions. Deposition of C 5b−9 within the epidermis correlated with a diagnosis of SCLE with or without antibodies to Ro and was seen in SLE patients with antibodies to extractable nuclear antigens Ro. La, Sm. and RNP. and in DLE patients with positive antinuclear antibodies and/or extracutaneous manifestations. In the SLE group, vascular C 5b−9 deposition was present in six patients. Of these, tour had circulating lupus anticoagulant, one had lymphocytic vasculitis, and two had antibodies to Ro. In two patients with SLE there was keratinocyte decoration for immunoglobulin G but not for C 5b−9 , in the absence of seropositivity for antibodies to Ro. La. Sm. and ribonucleoprotein (RNP). The immunohistological examination of skin lesions using a monoclonal antibody to C 5b−9 is a valuable adjunct in the subclassification of LE. The presence of C 5b−9 within skin lesions of patients with LE implies a pathogenic role for complement‐mediated pore formation.