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Related Experiment Video

Updated: May 29, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Pemphigus autoimmunity: hypotheses and realities.

Sergei A Grando¹

¹Department of Dermatology, University of California, Irvine, CA 92697, USA. sgrando@uci.edu

|September 24, 2011

Summary

Pemphigus vulgaris and pemphigus foliaceus research aims for corticosteroid-free remission. Understanding keratinocyte death mechanisms reveals new treatment avenues beyond traditional views.

Area of Science:

Dermatology and Immunology
Molecular Pathogenesis of Autoimmune Blistering Diseases

Background:

Pemphigus vulgaris and pemphigus foliaceus are autoimmune diseases characterized by blistering.
Current research aims to achieve clinical remission without corticosteroids.

Purpose of the Study:

To review recent advances in understanding pemphigus autoimmunity and its implications for treatment.
To explore novel perspectives challenging the monopathogenic explanation of disease immunopathology.

Main Methods:

Review of current literature on pemphigus pathogenesis, focusing on keratinocyte detachment and death.
Analysis of molecular mechanisms involving autoantibodies, intracellular signaling pathways, and cell death effectors.

Main Results:

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Granulocyte-dependent Autoantibody-induced Skin Blistering

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Published on: October 12, 2012

Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity

Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity

Published on: April 11, 2019

Generation of Two-color Antigen Microarrays for the Simultaneous Detection of IgG and IgM Autoantibodies

Generation of Two-color Antigen Microarrays for the Simultaneous Detection of IgG and IgM Autoantibodies

Published on: September 15, 2016

Pemphigus autoimmunity targets over 50 antigens, including desmosomal cadherins and cell membrane receptors.
Autoantibodies trigger intracellular signaling cascades leading to keratinocyte shrinkage, desmosome loss, and cell death (apoptolysis).
Synergy between autoantibodies and apoptotic/inflammatory pathways activates keratinocyte cell death programs.

Conclusions:

Elucidation of pemphigus immunopathology challenges previous disease models.
Advances in understanding molecular mechanisms facilitate the development of steroid-sparing therapies.
Further research into immune dysregulation and apoptolysis is crucial for developing steroid-free treatments.