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SHR Neuro Cancer Cardio Lipid Metab Microb
Numata, T; Shia, M; Nakamura, Y; Li, F; Chan, H; Nakatsuji, T; Cavagnero, KJ; Simmons, J; Li, H; Joshi, AA; Palomo-Irigoyen, M; Gallo, RL.
Dermal fibroblasts respond to interleukin-4 and 13 and promote T-cell recruitment in atopic dermatitis.
J Clin Invest. 2026;
Doi: 10.1172/JCI196108
PubMed
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- Authors Med Uni Graz:
- Joshi Aaroh Anand
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- Abstract:
- Atopic dermatitis (AD) is a chronic inflammatory skin condition characterized by a type 2 immune response that is not fully understood. Single-cell RNA sequencing (scRNA-seq) of human AD skin and murine models of type 2 inflammation identified transcriptionally distinct fibroblast clusters, revealing unique, IL-4Rɑ-dependent populations of immune-acting fibroblasts. These unbiased findings prompted further investigation into the role of dermal fibroblasts during allergic inflammation. These studies demonstrated that, in an inflammatory environment including TNFɑ, IL-1β and IL-17A, IL-4 and IL-13 stimulate both mouse and human fibroblasts to produce multiple chemokines, including Ccl8, which activates Ccr3 to attract T-cells. In the skin, fibroblasts are the primary source of many of these chemokines, and targeted deletion of IL--4rɑ in mouse fibroblasts reduces T-cell infiltration in a mouse model of AD. Additionally, pharmacologic inhibition of Ccr3, the receptor shared by many chemokines produced by fibroblasts, decreases T-cell infiltration and skin inflammation in AD mouse models. These findings demonstrate that dermal fibroblasts are more than passive structural cells; they actively participate in the type 2 immune response and contribute to AD by producing chemokines that increase inflammation. Targeting the functions of immune-acting fibroblasts could offer an alternative therapeutic approach for AD.