title: Further evidence for involvement of both cell mediated and humoral immunity in generalized vitiligo.
abstract: Immunohistochemical and immunoserological evidence supports the involvement of both cell-mediated and humoral mechanisms in the pathogenesis of melanocyte destruction in vitiligo. Punch biopsies from depigmented vitiliginous skin (VS), normal-looking pigmented skin (PS), and marginal skin (MS) from patients with generalized vitiligo (n = 15) were labeled with K 1.2.58, OKM1 (CD11b), Leu 11b (CD16), Leu 19 (CD56), IFN-gamma receptor, IL-2 receptor (CD25), IgG, IgM, C3c, and C3d MoAbs. In addition, in vitro effects of vitiligo sera (n = 13) on human newborn melanocytes (HMel) under different culture conditions were studied. The immunohistochemical findings showed absence of K 1.2.58+ epidermal melanocytes in VS and abnormal morphology in MS. In these areas, a few CD11b+ cells in the dermis and epidermis could be detected but no significant numbers of CD16+ or CD56+ cells were seen among the mononuclear cellular infiltrate. IL-2 and IFN-gamma receptors were clearly expressed by the cellular infiltrate. No significant deposition of complement or immunoglobulin was seen. The addition of vitiligo sera to HMel cultures induced a significant cellular proliferation. The stimulation of cell proliferation occurred regardless whether the sera were added alone or when preheated (56 degrees C for 1 hr) and then supplemented with a complement source (P < 0.01 at 2%, P < 0.001 at 10%, and P < 0.01 at 20% for sera alone) (P > 0.05 at 2%, P < 0.05 at 10%, and P < 0.01 at 20% for decomplemented sera plus complement).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Dermatology, Medical Center Steglitz, Free University of Berlin, Germany.
authors.forename: M B
authors.initials: MB
authors.lastname: Abdel-Naser
authors.forename: S
authors.initials: S
authors.lastname: Krüger-Krasagakes
authors.forename: K
authors.initials: K
authors.lastname: Krasagakis
authors.forename: H
authors.initials: H
authors.lastname: Gollnick
authors.forename: A
authors.initials: A
authors.lastname: Abdel-Fattah
authors.forename: C E
authors.initials: CE
authors.lastname: Orfanos
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000276:immunology; D000917:Antibody Formation; D000920:Antibody-Dependent Cell Cytotoxicity; D015703:Antigens, CD / Q000032:analysis; D015415:Biomarkers; D001706:Biopsy; D001769:Blood / Q000276:immunology; D002478:Cells, Cultured; D003165:Complement System Proteins / Q000276:immunology / Q000494:pharmacology; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007231:Infant, Newborn; D008213:Lymphocyte Activation; D008297:Male; D008544:Melanocytes / Q000276:immunology / Q000473:pathology; D008875:Middle Aged; D011947:Receptors, Antigen, B-Cell / Q000032:analysis; D017471:Receptors, Interferon / Q000032:analysis; D015375:Receptors, Interleukin-2 / Q000032:analysis; D014820:Vitiligo / Q000097:blood / Q000276:immunology* / Q000473:pathology; D000096743:Interferon gamma Receptor
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015415:Biomarkers; D003165:Complement System Proteins; D011947:Receptors, Antigen, B-Cell; D017471:Receptors, Interferon; D015375:Receptors, Interleukin-2; D000096743:Interferon gamma Receptor