Pemphigus & Pemphigoid Diseases

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Pemphigus and pemphigoid disease models: accelerate your preclinical pipeline

Pemphigus and pemphigoid are rare, chronic autoimmune blistering diseases in which autoantibodies target structural proteins in the skin and/or mucous membranes, leading to loss of adhesion and blister formation.

  • Pemphigoid diseases are characterized by autoantibodies against hemidesmosomal proteins at the dermal–epidermal junction, driving immune-cell recruitment, inflammation, and subepidermal splitting.
  • Pemphigus diseases are characterized by autoantibodies against desmosomal proteins, resulting in loss of keratinocyte–keratinocyte adhesion and intraepidermal blistering.

Because existing therapies can be limited by relapse and systemic side effects, there is strong demand for safer and more targeted treatment strategies—and for translational assay systems that can help teams evaluate candidate therapeutics efficiently in human-relevant settings.

Interested in learning how we can support your drug discovery and development? Learn more below.

Note: The assay platform described below is currently focused on pemphigoid diseases.

Related Publications

SELECTED PUBLICATIONS:

Pemphigoid disease model systems for clinical translation

>> Check the full list HERE.

Conference Contributions

We share our research on dermatology and trichology through international conferences and publications, contributing to the advancement of research in these fields.

>> Check our past contributions HERE.

What we help you achieve

  • Evaluate candidate therapeutics against key pemphigoid effector mechanisms (neutrophil activation and complement activation).
  • Generate mechanism-focused preclinical evidence to support lead selection and early proof-of-concept.
  • Benchmark candidates against current therapies within a controlled assay framework.
  • Reduce reliance on animal studies by filtering and prioritizing compounds using human skin and donor-derived cells.

In Vitro Models for Pemphigoid Diseases

  • ROS-release assay: Measures reactive oxygen species from human neutrophils upon immune-complex activation. Ideal for screening anti-inflammatory small molecules.
  • Cryosection assay: Human skin cryosections incubated with patient or recombinant IgG to quantify dermal–epidermal split formation. Validates mechanism in a tissue context.
  • Complement fixation assay: Fluorescence-labeled C3/C5 antibody binding to immune complexes on skin sections. Perfect for pipeline testing of complement inhibitors.

Ex Vivo Models for Pemphigoid Diseases

  • Human skin blistering model: Full-thickness human skin explants incubated with autoantibodies and neutrophils to replicate subepidermal blister formation.
  • 3D skin equivalents: Organotypic cultures with keratinocytes, fibroblasts, and immune cells for dynamic testing of compound penetration and efficacy.

Pemphigoid Disease Models Available Now (in vitro & ex vivo)

IMMUNE COMPLEX-INDUCED NEUTROPHIL ACTIVATION

Test: ROS-release assay (AUC readout)

What it measures: Reactive oxygen species (ROS) release from immune complex–activated neutrophils.
Assay principle:

  1. Immune complex (IC) formed on a plate using an autoantibody and its corresponding antigen
  2. Neutrophils isolated from healthy blood donors are added
  3. ROS-driven luminol chemiluminescence is measured
  4. Neutrophil activation is quantified from the area under the luminescence curve (AUC)

Use case: Screening and ranking compounds based on their ability to reduce neutrophil activation.

NEUTROPHIL-DRIVEN DERMAL-EPIDERMAL JUNCTION DAMAGE

Test: Cryosection split assay

What it measures: Split formation at the dermal–epidermal junction (DEJ) in human skin sections.
Assay principle:

  1. Incubate healthy human skin sections with autoantibodies
  2. Incubate with neutrophils isolated from healthy blood donors
  3. Split formation is induced at the DEJ
  4. Readout is the percentage of split formation

Use case: Tissue-level confirmation of functional protection beyond cell-based readouts.

COMPLEMENT BINDING AND ACTIVATION AT THE DEJ

Test: Complement fixation assay (C3c immunofluorescence)

What it measures: Complement deposition along the DEJ via autoantibody-mediated fixation.
Assay principle:

  1. Incubate healthy human skin sections with autoantibodies, then with normal human serum (complement source)
  2. Complement components are fixed to the DEJ
  3. Detection is performed using a fluorescence-labelled anti-complement C3c antibody
  4. Readout is fluorescence intensity along the DEJ (inhibition assessed as reduced signal)

Use case: Testing complement-pathway intervention strategies in a human tissue context.

Models Under Development

  • New ex vivo platforms for pemphigoid diseases – coming soon!
  • Additional assays for pemphigus indications – contact us for details.

At QIMA Life Sciences, we are committed to staying at the forefront of dermatology research by developing innovative approaches.

We offer smart solutions for studying pemphigus and pemphigoid diseases using validated models, making us the perfect partner for your research.

Explore Our Models & Assays in Our Flyer and Poster

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