Results 11 to 20 of about 7,948 (164)
Expression of Desmoglein 1 Compensates for Genetic Loss of Desmoglein 3 in Keratinocyte Adhesion [PDF]
Journal of Investigative Dermatology, 2002 The desmoglein compensation hypothesis, namely that one desmoglein can compensate for loss of function of another, has been proposed to explain the tissue specificity of the autoantibody-induced loss of cell adhesion in pemphigus. To validate this hypothesis genetically, we used desmoglein-3 knockout mice (DSG3-/-) that lose their telogen hair ...
Hanakawa, Yasushi +2 more
openaire +3 more sources
Journal of Investigative Dermatology, 1997 Pemphigus vulgaris and pemphigus foliaceus are cutaneous autoimmune diseases characterized by intraepithelial blisters and autoantibodies to desmosomal glycoproteins. The antigens recognized by pemphigus vulgaris and pemphigus foliaceus autoantibodies are desmoglein-3 (Dsg3) and desmoglein-1 (Dsg1), respectively.
Lin, Mong-Shang +5 more
openaire +3 more sources
Indian Journal of Dermatology, 2016 Pemphigus vulgaris (PV) is an autoimmune blistering disease elicited by anti-desmoglein (DsG) 3 antibody. Although skin lesions tend to be distributed over the entire body, in some patients, they are confined to a restricted area. We report two patients who presented with long-lasting localized PV without detectable anti-DsG antibodies after suffering ...
Asuka Yoshifuku +7 more
openaire +4 more sources
Desmoglein-3 autoantibodies in tissues of oral lichen planus patients and its correlation with disease severity: case-control study. [PDF]
BMC Oral HealthBackground Due to the not fully understood exact pathogenesis of oral lichen planus, the patients receive symptomatic management, rather than a curative treatment.
Abdelwadood D +3 more
europepmc +2 more sources
Binding to the neonatal Fc receptor enhances the pathogenicity of anti-desmoglein-3 antibodies in keratinocytes. [PDF]
Front ImmunolThe neonatal Fc receptor (FcRn) is important for numerous cellular processes that involve antibody recycling and trafficking. A major function of FcRn is IgG recycling and half-life prolongation, and FcRn blockade results in a reduction of autoantibodies
Zakrzewicz A +6 more
europepmc +3 more sources
Monovalent antibody-conjugated lipid-polymer nanohybrids for active targeting to desmoglein 3 of keratinocytes to attenuate psoriasiform inflammation. [PDF]
Theranostics, 2021 journal ...
Lin ZC +5 more
europepmc +2 more sources
Clinical periodontal diagnosis
Periodontology 2000, EarlyView., 2023 Abstract Periodontal diseases include pathological conditions elicited by the presence of bacterial biofilms leading to a host response. In the diagnostic process, clinical signs such as bleeding on probing, development of periodontal pockets and gingival recessions, furcation involvement and presence of radiographic bone loss should be assessed prior ...
Giovanni E. Salvi +5 more
wiley +1 more source
Archives of Dermatology, 1999 Pemphigus vulgaris (PV) is an autoimmune-blistering disease of the skin and mucous membranes caused by autoantibodies against desmoglein 3 (Dsg3), an epidermal desmosomal adhesion protein of the cadherin family. Cloning of the Dsg3 gene and expression of the protein in a native conformation enabled the recent development of a specific and sensitive ...
P, Lenz +4 more
openaire +2 more sources
Pemphigus IgG Causes Skin Splitting in the Presence of Both Desmoglein 1 and Desmoglein 3 [PDF]
The American Journal of Pathology, 2007 According to the desmoglein (Dsg) compensation concept, different epidermal cleavage planes observed in pemphigus vulgaris and pemphigus foliaceus have been proposed to be caused by different autoantibody profiles against the desmosomal proteins Dsg 1 and Dsg 3.
Volker, Spindler +3 more
openaire +2 more sources
Suppression of the Immune Response Against Exogenous Desmoglein 3 in Desmoglein 3 Knockout Mice: An Implication for Gene Therapy [PDF]
Journal of Investigative Dermatology, 2003 Gene therapies for recessive genetic diseases may provoke unwanted immune responses against the introduced gene product because patients, especially those with null mutation of a certain protein, have no tolerance for the protein of interest. This study used desmoglein 3 knockout (Dsg3-/-) mice as a disease model for a genetic defect in DSG3, to ...
Ohyama, Manabu +7 more
openaire +2 more sources