Antibodies against desmoglein 3 (pemphigus vulgaris antigen) are present in sera from patients with paraneoplastic pemphigus and cause acantholysis in vivo in neonatal mice.
نویسندگان
چکیده
منابع مشابه
Antibodies against desmoglein 3 (pemphigus vulgaris antigen) are present in sera from patients with paraneoplastic pemphigus and cause acantholysis in vivo in neonatal mice.
Paraneoplastic pemphigus (PNP) is an autoimmune blistering disease that occurs in association with underlying neoplasms. Patients with PNP develop characteristic IgG autoantibodies directed against multiple antigens, most of which have been identified as cytoplasmic proteins of the plakin family (desmoplakin I, II, BPAG1, envoplakin, and periplakin). This study identified cell surface target an...
متن کاملPemphigus vulgaris acantholysis ameliorated by cholinergic agonists.
BACKGROUND Pemphigus vulgaris (PV) is an autoimmune, IgG autoantibody-mediated disease of skin and mucosa leading to progressive blistering and nonhealing erosions. Patients develop autoantibodies to adhesion molecules mediating intercellular adhesion and to keratinocyte cholinergic receptors regulating cell adhesion. OBSERVATIONS To determine whether a cholinergic agonist can abolish PV IgG-...
متن کاملDo serum prolactin levels correlate with antibodies against desmoglein in pemphigus vulgaris?
BACKGROUND Pemphigus vulgaris is a chronic inflammatory disease of skin, the etiology of which is not completely known. Despite the latter, anti-desmoglein antibodies play a proven role in the pathogenesis. Recent studies showed an etiologic effect for prolactin in the pemphigus vulgaris. This study aimed to quantify the correlation between serum prolactin levels and anti-desmoglein antibodies ...
متن کاملPathogenic IgG antibodies against desmoglein 3 in pemphigus vulgaris are regulated by HLA-DRB1*04:02-restricted T cells.
Pemphigus vulgaris (PV) is considered as a model for an autoantibody-mediated organ-specific autoimmune disorder. IgG autoantibodies directed against the desmosomal cadherin desmoglein 3 (Dsg3), the major autoantigen in PV, cause loss of epidermal keratinocyte adhesion, resulting in blisters and erosions of the skin and mucous membranes. The association of human autoimmune diseases with distinc...
متن کاملTargeted Disruption of the Pemphigus Vulgaris Antigen (Desmoglein 3) Gene in Mice Causes Loss of Keratinocyte Cell Adhesion with a Phenotype Similar to Pemphigus Vulgaris
In patients with pemphigus vulgaris (PV), autoantibodies against desmoglein 3 (Dsg3) cause loss of cell-cell adhesion of keratinocytes in the basal and immediate suprabasal layers of stratified squamous epithelia. The pathology, at least partially, may depend on protease release from keratinocytes, but might also result from antibodies interfering with an adhesion function of Dsg3. However, a d...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Clinical Investigation
سال: 1998
ISSN: 0021-9738
DOI: 10.1172/jci3647