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Aberrant expression of complement regulatory proteins, membrane cofactor protein and decay accelerating factor, in the involved epidermis of patients with vitiligo
Author(s) -
Van Den Wijngaard R.M.J.G.J.,
Asghar S.S.,
Pijnenborg A.C.L.M.,
Tigges A.J.,
Westerhof W.,
Das P.K.
Publication year - 2002
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.1365-2133.2002.04604.x
Subject(s) - vitiligo , decay accelerating factor , biology , melanocyte , cd46 , complement system , epidermis (zoology) , immunohistochemistry , complement factor i , microbiology and biotechnology , immunology , pathology , cancer research , antibody , medicine , melanoma , anatomy
Summary Background Vitiligo is a pigmentary disorder of the skin characterized by the complete absence of melanocytes from the lesion. Complement‐activating antimelanocyte antibodies have been implicated in vitiligo pathogenesis. As membrane regulators of complement activation, membrane cofactor protein, decay accelerating factor and CD59 protect cells from elimination by autologous complement, their absence or downregulation on melanocytes may be associated with autoantibody and complement‐mediated melanocyte destruction in vitiligo. Objectives We studied the expression of these regulatory proteins in non‐lesional, perilesional and lesional vitiligo skin compared with those of control specimens. Methods We used immunohistochemistry to study the expression of the regulatory proteins, and flow cytometric analysis of cultured melanocytes to investigate possible constitutive changes in the expression levels of these molecules. We also investigated whether melanocytes can influence keratinocyte susceptibility to autologous complement by regulating keratinocytic decay accelerating factor and membrane cofactor protein expression levels. Results Immunohistochemical data showed that expression of membrane cofactor protein and decay accelerating factor in whole epidermis was lower in lesional and perilesional skin in comparison with non‐lesional skin. The reduced in situ expression appeared to be specific to vitiligo. However, coculture experiments indicated that melanocytes do not influence keratinocyte susceptibility to autologous complement. Further, flow cytometric analysis of cultured melanocytes convincingly demonstrated that non‐lesional vitiligo and control melanocytes have comparable decay accelerating factor, membrane cofactor protein and CD59 expression levels. Conclusions It is therefore concluded that there is no constitutive melanocyte defect per se that could be related to the in vivo expression of these molecules in vitiligo. Nevertheless, the present data suggest that both keratinocytes and melanocytes in the involved vitiliginous whole epidermis express lower levels of decay accelerating factor and membrane cofactor protein compared with controls that could render them more vulnerable to autologous complement attack.