Aberrant expression of complement regulatory proteins, membrane cofactor protein and decay accelerating factor, in the involved epidermis of patients with vitiligo
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W. Westerhof | P. Das | A. Tigges | R. M. van den Wijngaard | A. Pijnenborg | R. Wijngaard | S. S. Asghar | R.M.J.G.J. Van Den Wijngaard | S.S. Asghar | A.C.L.M. Pijnenborg | P.K. Das | R.M.J.G.J. Van Den Wijngaard | Pranal Das | A.C.L.M. Pijnenborg
[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.