Inflammatory Skin Disease Research

Human ex vivo models for inflammatory skin disease research

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Generate human-relevant data for better-informed dermatology drug development

Genoskin

Inflammatory skin diseases such as psoriasis, atopic dermatitis (AD) and hidradenitis suppurativa (HS) involve complex interactions between immune signaling, resident immune cells and epidermal biology. Studying these mechanisms in real human tissue helps drug developers make better-informed decisions before clinical trials.

Genoskin is a contract research organization (CRO) specializing in human ex vivo skin. Our studies capture three distinct inflammatory mechanisms. For psoriasis and AD, we induce T cell–driven Th1/Th17 inflammation or type 2 cytokine–driven barrier impairment in healthy human skin. For HS, we work directly with diseased skin from patients. Every study preserves native skin architecture and resident immune cells, and uses multiparametric readouts to evaluate your drug candidates.

Explore our inflammatory skin disease models

psoriasis

Psoriasis

Test biologics and small molecules, applied topically, systemically or by injection. InflammaSkin® activates resident T cells in native human skin to reproduce early Th1/Th17 psoriatic inflammation, so you can measure how your candidate suppresses it.

Explore psoriasis studies →

Atopic dermatitis

Atopic dermatitis

Test topical therapeutics in our type 2 barrier impairment study. IL-4 and/or IL-13 stimulation of native human skin reproduces the barrier dysfunction seen in AD, so you can measure how your candidate restores barrier function.

Explore atopic dermatitis studies →

hidradenitis suppurativa

Hidradenitis suppurativa

Test biologics, small molecules and topicals directly in skin from HS patients. Biostabilized lesional tissue preserves the disease’s own architecture and immune environment, so you can measure drug responses in real diseased skin.

Explore HS studies →

Which inflammatory pathway are you targeting?

Tell us your indication, modality, target, formulation constraints and the decision you need to make. We’ll propose a study design aligned to your program.

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Select, rank and advance your next dermatology candidate

Each study answers a different question. Use the comparison below to match your mechanism, modality and administration route to the right design.

These approaches enable the assessment of therapeutic responses and disease-relevant biomarkers in native human skin, generating translational data to support drug development. While preserving key aspects of local skin biology, these models do not reproduce the full complexity of disease in vivo, including systemic immune responses.

Frequently asked questions

Which human skin model is best for psoriasis, atopic dermatitis, or hidradenitis suppurativa research?

Genoskin offers three complementary human ex vivo approaches: InflammaSkin® for Th1/Th17-driven psoriasis-like inflammation, a type-2 cytokine-induced model for atopic dermatitis (AD)-associated barrier impairment, and patient-derived hidradenitis suppurativa (HS) skin models. The best choice depends on your therapeutic target, disease mechanism, and research objectives.

Why use human ex vivo skin models for inflammatory skin disease research?

Human ex vivo skin models preserve native tissue architecture and relevant resident immune cell populations, enabling researchers to evaluate inflammatory responses and therapeutic effects directly in human tissue. They provide complementary human-relevant data for preclinical drug development, although they do not fully reproduce systemic disease processes.

What types of therapeutic candidates and biomarkers can be evaluated?

Depending on the model, Genoskin can evaluate biologics, small molecules, and topical formulations through multiplex cytokine profiling, histology, immunostaining, transcriptomics, flow cytometry and enzyme-based functional assays. Studies can be designed for dose-response assessment, candidate comparison, mechanism-of-action investigation, and therapeutic efficacy evaluation.

What is InflammaSkin® and how does it reproduce psoriasis-like inflammation?

InflammaSkin® is a human ex vivo skin model that reproduces key features of early psoriasis-like inflammation through activation of resident T cells. It generates a Th1/Th17-driven inflammatory response while preserving native human skin architecture, providing a platform for evaluating anti-psoriatic therapies.

Can InflammaSkin® be used to evaluate biologics and anti-inflammatory treatments?

Yes. InflammaSkin® supports testing of biologics and small molecules through topical application, injection, or culture medium exposure, depending on the compound. Genoskin has demonstrated treatment-associated reductions in psoriasis-related inflammatory cytokines following exposure to reference therapies.

Which inflammatory biomarkers can be measured in InflammaSkin® studies?

InflammaSkin® studies can assess psoriasis-associated cytokines such as IL-17A, IL-22, IFN-γ, and TNF-α, alongside immune activation (CD69) and proliferation (Ki-67) markers. Additional tissue-level and molecular analyses can help characterize inflammatory responses and therapeutic effects.

How does Genoskin's AD-like model reproduce atopic dermatitis-associated skin barrier dysfunction?

Genoskin’s AD-like model uses native human skin stimulated with IL-4 and/or IL-13 to induce type-2 inflammatory signaling and epidermal barrier impairment. These cytokines alter barrier-associated gene and protein expression, reproducing key features of atopic dermatitis-related skin dysfunction.

Can the AD-like model evaluate the efficacy of topical treatments for atopic dermatitis?

Yes. The model is designed to evaluate topical therapeutic candidates by measuring their ability to improve epidermal barrier function and modulate type-2 inflammation-associated molecular pathways. It supports early-stage compound screening, formulation comparison, and candidate selection.

How is skin barrier recovery measured in the AD-like model?

Barrier function can be assessed using electrical impedance spectroscopy (EIS), which measures changes in epidermal barrier integrity. Complementary readouts include filaggrin (FLG) protein expression, barrier-associated gene expression, and transcriptomic profiling to characterize treatment effects.

How does Genoskin's hidradenitis suppurativa model differ from induced inflammatory skin models?

Unlike cytokine-induced inflammatory models, Genoskin’s HS platform uses skin collected from patients with hidradenitis suppurativa, including lesional tissue. The biostabilized ex vivo model preserves disease-associated tissue architecture and relevant cellular components, allowing researchers to study therapeutic responses directly in human disease skin.

Can Genoskin's HS skin model be used to evaluate new therapies for hidradenitis suppurativa?

Yes. Genoskin offers customized treatment-response studies using biostabilized human HS skin to evaluate biologics, small molecules, and topical candidates. The platform supports dose-response testing, mechanism-of-action studies, and comparisons with reference treatments.

Which biomarkers and readouts are available for hidradenitis suppurativa research?

HS studies can incorporate inflammatory biomarker profiling, histological assessment, transcriptomic analysis and spatial immune cell characterization. These complementary readouts enable the assessment of inflammatory activity, tissue architecture, immune cell populations and molecular changes within diseased skin tissue, as well as responses to therapeutic interventions.