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Related Concept Videos

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The term desmosome derives from the Greek words "desmo" and "soma" meaning "adhesion bodies." This structure was first observed during the late 1800s and described as small, dense nodules in the epidermis. Desmosomes are button-like structures that help form an interlinked network of intermediate filaments across the cells. These junctions are  essential to hold cells together under mechanical stress and to maintain tissue integrity. Desmosomes are multi-protein...
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Skin is the first line of defense and encounters a variety of microbes. Some pathogenic strains are often the cause of a broad range of infections of the skin and other body systems. These conditions can affect people of all ages and may have different causes, including genetic factors, infections, autoimmune reactions, environmental factors, and lifestyle choices.
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Related Experiment Video

Updated: Mar 2, 2026

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid
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Pemphigus.

Michael Kasperkiewicz1, Christoph T Ellebrecht2, Hayato Takahashi3

  • 1Department of Dermatology, University of Lübeck, Lübeck, Germany.

Nature Reviews. Disease Primers
|May 12, 2017
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Summary
This summary is machine-generated.

Pemphigus is an autoimmune disease causing blisters due to IgG antibodies targeting desmogleins. Research clarifies its mechanisms and treatments, including rituximab, offering hope for targeted therapies.

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Area of Science:

  • Immunodermatology
  • Autoimmune diseases
  • Cell adhesion biology

Background:

  • Pemphigus is an IgG-mediated autoimmune disease affecting stratified squamous epithelia.
  • Characterized by acantholysis, leading to skin and mucosal blisters.
  • Key subtypes include pemphigus vulgaris, pemphigus foliaceus, and paraneoplastic pemphigus.

Purpose of the Study:

  • To elucidate the pathophysiology of pemphigus.
  • To review diagnostic and therapeutic strategies.
  • To highlight pemphigus as a model for autoimmune disease research.

Main Methods:

  • Review of clinical manifestations, histology, and immunochemical testing.
  • Analysis of autoantibody profiles against desmoglein 1 and desmoglein 3.
  • Characterization of T cell and B cell roles in pathogenesis.

Main Results:

  • Autoantibodies against desmogleins are central to blister formation.
  • Tissue-specific desmoglein expression correlates with lesion sites.
  • Mouse models and patient studies reveal autoimmune mechanisms.

Conclusions:

  • Pemphigus pathogenesis is linked to anti-desmoglein autoantibodies.
  • Current treatments involve corticosteroids and immunosuppressants; rituximab shows promise.
  • Pemphigus serves as a key model for developing antigen-specific autoimmune therapies.