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Pemphigus vulgaris autoimmune globulin induces Src-dependent tyrosine-phosphorylation of plakophilin 3 and its detachment from desmoglein 3.
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The cell adhesion molecule plakophilin 3 (Pkp3) plays an essential role in the maintenance of skin integrity and is targeted in certain autoimmune conditions. In one example, we have shown that Pkp3 is instrumental in mediating the discohesive effects of sera from patients with pemphigus vulgaris
Abl family tyrosine kinases govern IgG extravasation in the skin in a murine pemphigus model.
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The pathway of homeostatic IgG extravasation is not fully understood, in spite of its importance for the maintenance of host immunity, the management of autoantibody-mediated disorders, and the use of antibody-based biologics. Here we show in a murine model of pemphigus, a prototypic cutaneous
Efficacy of a Bruton's Tyrosine Kinase Inhibitor (PRN-473) in the treatment of canine pemphigus foliaceus.
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Open trial of Bruton's tyrosine kinase inhibitor (PRN1008) in the treatment of canine pemphigus foliaceus
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Background: Bruton's tyrosine kinase (BTK) is important in B-cell signalling. Efficacy has been reported for BTK inhibitors (BTKi) in human autoimmune diseases. Canine pemphigus foliaceus (cPF) is one of the most common canine autoimmune
Pemphigus foliaceous-like reaction in a patient with chronic myeloid leukemia treated with the tyrosine kinase inhibitors nilotinib and dasatinib.
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[Blood tyrosine level--a criterion of the optimal glucocorticoid therapy of patients with pemphigus].
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[Tyrosine content of the blood in pemphigus].
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Differential coupling of M1 muscarinic and alpha7 nicotinic receptors to inhibition of pemphigus acantholysis.
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The mechanisms mediating and regulating assembly and disassembly of intercellular junctions is a subject of intensive research. The IgG autoantibodies produced in patients with the immunoblistering skin disease pemphigus vulgaris (PV) can induce keratinocyte (KC) dyshesion (acantholysis) via
Paraneoplastic Pemphigus Associated with B-cell Chronic Lymphocytic Leukemia Treated with Ibrutinib and Rituximab.
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Paraneoplastic pemphigus (PNP) is a severe autoimmune blistering disease associated with an underlying malignancy, and its prognosis is poor. We herein report the first patient with B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma (B-CLL/SLL)-associated PNP successfully treated with
Pemphigus foliaceus and desmoglein 1 gene polymorphism: is there any relationship?
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Transmembrane proteins of the cadherin superfamily, the desmogleins and desmocollins, mediate intercellular adhesion in desmosomes. Autoantibodies to desmoglein 1 (dsg1) are a hallmark of pemphigus foliaceus (PF), a disease characterized by skin blistering resulting from keratinocyte cell
Pemphigus vulgaris IgG cause loss of desmoglein-mediated adhesion and keratinocyte dissociation independent of epidermal growth factor receptor.
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Autoantibody-induced cellular signaling mechanisms contribute to the pathogenesis of autoimmune blistering skin disease pemphigus vulgaris (PV). Recently, it was proposed that epidermal growth factor receptor (EGFR) might be involved in PV signaling pathways. In this study, we investigated the role
Apoptotic mechanism in pemphigus autoimmunoglobulins-induced acantholysis--possible involvement of the EGF receptor.
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Pemphigus is an autoimmune cutaneous disease characterized by circulating autoantibodies that cause blistering and erosions on skin and mucous membranes. Circulating autoantibodies bind to epidermal cell membrane and cause cell-cell detachment (acantholysis), leading to epidermal tissue damage and
In vivo blockade of pemphigus vulgaris acantholysis by inhibition of intracellular signal transduction cascades.
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BACKGROUND
Pemphigus vulgaris (PV) is an autoimmune disease characterized by mucocutaneous intraepithelial blisters and pathogenic autoantibodies against desmoglein 3. The mechanism of blister formation in pemphigus has not been defined; however, in vitro data suggest a role for activation of
The role of nitric oxide synthases in pemphigus vulgaris in a mouse model.
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BACKGROUND
Pemphigus vulgaris (PV) is a blistering autoimmune disease characterized by IgG autoantibodies against desmoglein 3. Nitric oxide synthases (NOS) may contribute to the increase of inflammation in tissues by the generation of nitrotyrosine residues (NTR).
OBJECTIVE
To investigate whether
PTPN22 1858T is not a risk factor for North American pemphigus vulgaris.
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Alterations in the protein tyrosine phosphatase N22 (PTPN22) gene affect the threshold for lymphocyte activation. The PTPN22 1858T polymorphism leads to uninhibited T-cell receptor cascade propagation. An elevated PTPN22 1858C/T genotype frequency has been correlated with several autoimmune
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