Aberrant expression of complement regulatory proteins, membrane cofactor protein and decay accelerating factor, in the involved epidermis of patients with vitiligo

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.

[1]  A. Becker,et al.  Practical suggestions for successful immunoenzyme double-staining experiments , 2004, The Histochemical Journal.

[2]  Watson,et al.  Autoantibodies to tyrosinase‐related protein‐1 detected in the sera of vitiligo patients using a quantitative radiobinding assay , 1998, The British journal of dermatology.

[3]  M. Pasch,et al.  Complement as a promiscuous signal transduction device. , 1998, Laboratory investigation; a journal of technical methods and pathology.

[4]  G. Ogg,et al.  High Frequency of Skin-homing Melanocyte-specific Cytotoxic T Lymphocytes in Autoimmune Vitiligo , 1998, The Journal of experimental medicine.

[5]  W. Westerhof,et al.  Relative contributions of decay accelerating factor (DAF), membrane cofactor protein (MCP) and CD59 in the protection of melanocytes from homologous complement. , 1998, Immunobiology.

[6]  A. Houghton,et al.  A melanosomal membrane protein is a cell surface target for melanoma therapy. , 1996, Clinical cancer research : an official journal of the American Association for Cancer Research.

[7]  W. Westerhof,et al.  Presence of T cells and macrophages in inflammatory vitiligo skin parallels melanocyte disappearance. , 1996, The American journal of pathology.

[8]  A. Cattelan,et al.  Levels of cell membrane CD59 regulate the extent of complement-mediated lysis of human melanoma cells. , 1996, Laboratory investigation; a journal of technical methods and pathology.

[9]  Amos Etzioni,et al.  In vivo destruction of melanocytes by the IgG fraction of serum from patients with vitiligo. , 1995, The Journal of investigative dermatology.

[10]  A. Houghton,et al.  Implicating a role for immune recognition of self in tumor rejection: passive immunization against the brown locus protein , 1995, The Journal of experimental medicine.

[11]  W. Westerhof,et al.  Intrinsic regulators of complement activation in vitiligo , 1994 .

[12]  P. Das,et al.  Glycosylphosphatidylinositol (GPI)‐anchored membrane proteins are constitutively down‐regulated in psoriatic skin , 1994, The Journal of pathology.

[13]  C. Yu,et al.  Coexistence and relationship of antikeratinocyte and antimelanocyte antibodies in patients with non-segmental-type vitiligo. , 1993, The Journal of investigative dermatology.

[14]  J. Garioch,et al.  An immunohistological study of cutaneous lymphocytes in vitiligo , 1993, The Journal of pathology.

[15]  W. Westerhof,et al.  Presence or absence of melanocytes in vitiligo lesions: an immunohistochemical investigation. , 1993, The Journal of investigative dermatology.

[16]  W. Westerhof,et al.  Phagocytosis by normal human melanocytes in vitro. , 1993, Experimental cell research.

[17]  J. Bystryn,et al.  Relation between the incidence and level of pigment cell antibodies and disease activity in vitiligo. , 1991, The Journal of investigative dermatology.

[18]  J. Bystryn,et al.  Evidence for immunologic mechanisms in human vitiligo: patients' sera induce damage to human melanocytes in vitro by complement-mediated damage and antibody-dependent cellular cytotoxicity. , 1988, The Journal of investigative dermatology.

[19]  G. Naughton,et al.  THE SIGNIFICANCE OF VITILIGO ANTIBODIES , 1985, The Journal of dermatology.

[20]  G. Naughton,et al.  Antibodies to normal human melanocytes in vitiligo , 1983, The Journal of experimental medicine.

[21]  S. Hsu,et al.  Use of avidin-biotin-peroxidase complex (ABC) in immunoperoxidase techniques: a comparison between ABC and unlabeled antibody (PAP) procedures. , 1981, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[22]  A. Lerner On the etiology of vitiligo and gray hair. , 1971, The American journal of medicine.