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Updated: Feb 1, 2026

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
Published on: January 7, 2019
新生児皮膚における常在菌と骨髄球のクロストークは、インターロイキン-1シグナル伝達と皮膚の1型17炎症を調節する
Miqdad O Dhariwala1, Ricardo O Carale2, Andrea M DeRogatis2
1Department of Dermatology, University of California, San Francisco, San Francisco, CA, USA; Department of Microbial Infection and Immunity, Ohio State University, Columbus, OH, USA; Department of Dermatology, Ohio State University, Columbus, OH, USA.
Abstract:
Early-life microbe-immune interactions at barrier surfaces have lasting impacts on the trajectory toward 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 post-natal depletion of these monocytes resulted in heightened interleukin (IL)-17A production by skin T cells, which was particularly sustained among CD4+ T cells and was 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 of 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.
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