Protection against Pemphigus Foliaceus by Desmoglein 3 in Neonates
Hong Wu, M.D., Ph.D., Zhi Hong Wang, Albert Yan, M.D., Stephen Lyle, M.D., Ph.D., Steven Fakharzadeh, M.D., Ph.D., James K. Wahl, Margaret J. Wheelock, Ph.D., Hiroyasu Ishikawa, M.D., Ph.D., Jouni Uitto, M.D., Ph.D., Masayuki Amagai, M.D., Ph.D., and John R. Stanley, M.D.
Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.
Pemphigus foliaceus is an autoantibody-mediated blistering diseasein which antibodies against desmoglein 1 cause loss of adhesionamong keratinocytes in the superficial epidermis.1 Desmogleinsare transmembrane glycoproteins found in desmosomes, which providephysical connections between cells. The main desmogleins expressedin the epidermis are desmoglein 1 and desmoglein 3. In adults,desmoglein 1 is present throughout the epidermis, but desmoglein3 is present only in the basal and immediate suprabasal layers.2,3It has been proposed that in patients with pemphigus foliaceusthe antibodies interfere with the adhesive function of desmoglein1 and that blisters occur only in the superficial epidermis,. . . [Full Text of this Article]
Methods
Antibodies
Immunofluorescence Staining
Transgenic Mice
Results
Coexpression of Desmoglein 3 and Desmoglein 1 in Neonatal Epidermis
Ectopic Expression of Desmoglein 3 in the Superficial Epidermis
Discussion
Source Information
From the Department of Dermatology, University of Pennsylvania School of Medicine, Philadelphia (H.W., Z.H.W., A.Y., S.L., S.F., J.R.S.); the University of Toledo, Toledo, Ohio (J.K.W., M.J.W.); the Department of Dermatology and Cutaneous Biology, Jefferson Medical College, Philadelphia (H.I., J.U.); and the Department of Dermatology, Keio University School of Medicine, Tokyo, Japan (M.A.).
Address reprint requests to Dr. Stanley at the Department of Dermatology, University of Pennsylvania School of Medicine, 211B Clinical Research Bldg., 415 Curie Blvd., Philadelphia, PA 19104-6142.
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