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Commensal myeloid crosstalk in neonatal skin regulates cutaneous type 17 inflammation

GSE294110 Homo sapiens Expression profiling by high throughput sequencing 7 samples Submitted 2026/01/20 Platform GPL34284
Summary
Early life microbe-immune interactions at barrier surfaces have lasting impacts on the trajectory towards health versus disease. Monocytes, macrophages and dendritic cells are primary sentinels in barrier tissues, yet the salient contributions of commensal-myeloid crosstalk during tissue development remain poorly understood. Here, we identify that commensal microbes facilitate accumulation of a population of monocytes in neonatal skin. Transient postnatal depletion of these monocytes resulted in heightened IL-17A production by skin T cells, which was particularly sustained among CD4+ T cells into adulthood and sufficient to exacerbate inflammatory skin pathologies. Neonatal skin monocytes were enriched in expression of negative regulators of the IL-1 pathway. Functional in vivo experiments confirmed a key role for excessive IL-1R1 signaling in T cells as contributing to the dysregulated type 17 response in neonatal monocyte-depleted mice. Thus, a commensal-driven wave of monocytes into neonatal skin critically facilitates immune homeostasis in this prominent barrier tissue.
Published in
Commensal-myeloid crosstalk in neonatal skin regulates interleukin-1 signaling and cutaneous type 17 inflammation
Dhariwala MO, Carale RO, DeRogatis AM et al. · Immunity 2026 · PMID 41616767 · doi:10.1016/j.immuni.2026.01.005
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Also filed as BioProject PRJNA1248404 and SRA study SRP577412. Searching any of these in the dataset finder brings you back here.

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