What is it about?
We integrate emerging insights into atopic dermatitis to build a new preclinical model that captures key features of the disease, including epidermal barrier damage driven by skin dysbiosis, percutaneous allergen sensitization, neuroimmune interactions, and IL-22-mediated pathology. Using this atopic dermatitis model, we uncover novel molecular pathways, cellular states, and spatial features associated with allergic inflammation.
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Photo by Sasun Bughdaryan on Unsplash
Why is it important?
Drug development for atopic dermatitis remains heavily focused on targets that mediate type 2 immunity. However, the lesional skin of patients with atopic dermatitis reveals a complex immune landscape and points to disease-driving mechanisms that extend beyond type 2 immunity. Our findings reveal neuroimmune interactions and IL-22 signaling as key drivers of allergic skin inflammation and provide a mechanistic rationale for targeting these processes.
Perspectives
This work resulted from a collaboration among teams with expertise ranging from immunology and microbiology to biochemistry and bioinformatics. I look forward to seeing our findings translate into new therapies that address unmet clinical needs and benefit patients with atopic dermatitis.
Jin Mo Park
Harvard Medical School
Read the Original
This page is a summary of: The staphylococcal protease SspA perturbs the epidermal barrier and promotes IL-22-driven inflammation in allergen-exposed skin, Proceedings of the National Academy of Sciences, October 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2611563123.
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