Autoantibody Signaling in Pemphigus Vulgaris: Development of an Integrated Model

Frontiers in Immunology
Thomas Sajda, Animesh A Sinha

Abstract

Pemphigus vulgaris (PV) is an autoimmune skin blistering disease effecting both cutaneous and mucosal epithelia. Blister formation in PV is known to result from the binding of autoantibodies (autoAbs) to keratinocyte antigens. The primary antigenic targets of pathogenic autoAbs are known to be desmoglein 3, and to a lesser extent, desmoglein 1, cadherin family proteins that partially comprise the desmosome, a protein structure responsible for maintaining cell adhesion, although additional autoAbs, whose role in blister formation is still unclear, are also known to be present in PV patients. Nevertheless, there remain large gaps in knowledge concerning the precise mechanisms through which autoAb binding induces blister formation. Consequently, the primary therapeutic interventions for PV focus on systemic immunosuppression, whose side effects represent a significant health risk to patients. In an effort to identify novel, disease-specific therapeutic targets, a multitude of studies attempting to elucidate the pathogenic mechanisms downstream of autoAb binding, have led to significant advancements in the understanding of autoAb-mediated blister formation. Despite this enhanced characterization of disease processes, a satisfactory...Continue Reading

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Citations

Mar 9, 2019·Current Protocols in Pharmacology·Imke A K BurmesterJennifer E Hundt
Aug 21, 2020·British Journal of Pharmacology·Imke A K BurmesterRalf J Ludwig
Dec 24, 2019·Frontiers in Immunology·Desalegn Tadesse EguJens Waschke
Jan 29, 2021·Frontiers in Immunology·Katja BieberRalf J Ludwig
May 11, 2021·Autoimmunity Reviews·Cristian PaparaAdrian Baican
Apr 2, 2021·The British Journal of Dermatology·T SchmittJ Waschke

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Methods Mentioned

BETA
atomic force microscopy
AFM
environmental stress
GTPases

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