Atopic Dermatitis: The Skin’s Disease Memory (Medicine)

The presence of particular memory cells in the skin could explain why atopic dermatitis keeps recurring

Researchers from the Meduni Vienna and the CeMM were able to show that certain populations of immune cells settle in the skin of atopic dermatitis sufferers and are still present even after one year of successful therapy. These cells from the group of dendritic cells and T helper cells are characterized by the production of certain inflammatory messenger substances that fuel the activity of neurodermatitis.

Atopic dermatitis, also known as neurodermatitis or atopic eczema, is currently the most common chronic inflammatory skin disease in humans. It usually begins in early childhood and can be accompanied by food allergies, hay fever and allergic asthma. In many cases, the disease disappears again in late childhood or early adulthood, but a not inconsiderable proportion suffer from this very itchy skin disease for a lifetime. In these patients there are a number of therapy options to alleviate the skin symptoms or to bring them to healing, but atopic dermatitis usually returns very soon after the end of therapy.

Researchers at the University Clinic for Dermatology at MedUni Vienna (first author: Christine Bangert, project leader: Patrick M. Brunner), in collaboration with Thomas Krausgruber and Christoph Bock from CeMM, were able to show that certain populations of immune cells settle in the skin of atopic dermatitis sufferers, and these too cannot be eliminated after one year of successful therapy.

These cells, which belong to the group of dendritic cells and T helper cells, are characterized by the production of certain inflammatory messengers, which fuel the activity of neurodermatitis.

In the study, now published in the top journal Science Immunology, the authors examined skin samples from patients whose skin lesions had completely healed under therapy with the monoclonal antibody dupilumab, which blocks the interleukin-4 receptor. Despite the successful therapy, certain inflammatory cells, namely the dendritic and T-helper memory cells mentioned, were still detectable. Interestingly, these cells were not found in healthy volunteers.

“The fact that these cells do not appear to be found in healthy skin makes them an attractive target for new therapeutic approaches that could possibly lead to a long-term healing of this skin disease beyond active therapy,” explains Patrick Brunner. The so-called Th2A cells, which also occur in the blood of allergy sufferers and which disappear after successful immunotherapy, are of particular interest here. These cells have certain receptors on their surface that enable them to react quickly to inflammatory stimuli that are typical for diseases of the so-called atopic type (atopic dermatitis, asthma, allergic rhinitis). These cells could also contribute to why atopic dermatitis resolves spontaneously in adolescence in some patients, but persists for a lifetime in others.

Interestingly, increased inflammation signals were not only detectable in the skin, but also in the blood of successfully treated patients. “This result shows us that patients with severe atopic dermatitis also show systemic involvement due to successful therapy, despite the absence of appearance,” adds Christine Bangert.


Copyright of this article (English version) belongs to aur author S. Aman. One is allowed to reuse it only by giving proper credit either to him of to us.


Reference: Christine Bangert, Katharina Rindler, Thomas Krausgruber, Natalia Alkon, Felix M. Thaler, Harald Kurz, Tanya Ayub, Denis Demirtas, Nikolaus Fortelny, Vera Executive Lechner, Wolfgang M. Bauer, Tamara Quint, Michael Mildner, Constanze Jonak, Adelheid Elbe-Bürger, Johannes Griss, Christoph Bock, Patrick M. Brunner, “Persistence of mature dendritic cells, Th2A and Tc2 cells characterize clinically resolved atopic dermatitis under IL-4R-alpha blockade”, Science Immunology, Vol. 6, Issue 55, eabe2749 2021. DOI: 10.1126/sciimmunol.abe2749 https://immunology.sciencemag.org/content/6/55/eabe2749


Provided by Medical University of Vienna

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