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Dermal‐epidermal deposition of complement components and properdin in systemic lupus erythematosus
Author(s) -
JORDON ROBERT E.,
SCHROETER ARNOLD L.,
WINKELMANN R.K.
Publication year - 1975
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 - 10.1111/j.1365-2133.1975.tb03075.x
Subject(s) - properdin , complement system , medicine , antibody , pathology , deposition (geology) , skin lesion , alternative complement pathway , immunology , biology , paleontology , sediment
SUMMARY Skin lesions and clinically normal skin of thirteen patients with systemic lupus erythematosus (SLE) were examined, by the use of immunofluorescent techniques, to determine the presence of Ciq, C 3 , C 3 proactivator (C 3 PA), properdin, immunoglobulins (IgG, IgA, and IgM), and fibrin. IgM deposition was present in all thirteen skin lesions and in all eleven normal areas tested, whereas IgG deposition occurred in eleven of the lesions but in only six normal areas. IgA was the least frequently encountered immunoglobulin. C 1q deposition occurred in all thirteen skin lesions, and C 3 deposition was present in twelve. Seven of nine and eight of eleven clinically normal areas demonstrated C 1q and C 3 deposition, respectively. Although less intense than C 1q and C 3 deposition, properdin deposition occurred in eight of the thirteen skin lesions tested but in only two of nine normal areas. C 3 PA deposition was of greater intensity than was properdin, but was seen in only five lesions and three clinically normal areas. Seven skin lesions and two normal areas also demonstrated fibrin deposition. Although alternate pathway activation is. apparent, our findings suggest that the classical pathway (C 1 to C 9 ) is the primary complement pathway involved in slli skin.