Sociedad Americana de Hirudoterapia

Commensal-myeloid crosstalk in neonatal skin regulates interleukin-1 signaling and cutaneous type 17 inflammation

Research article published in Immunity (2026)

Última actualización: June 18, 2026Revisado por: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Preclinical (animal)Desarrollo de fármacosDhariwala MO et al. · Immunity, 2026

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.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal Article
Indexed MeSH termsAnimalsSkinMiceSignal TransductionAnimals, NewbornMonocytesMice, Inbred C57BLInterleukin-1Interleukin-17InflammationTh17 CellsMice, Knockout

Resumen

Early-life microbe-immune interactions at barrier surfaces have lasting impacts on the trajectory toward health versus disease.

Por qué esto importa para la hirudoterapia

This mouse study identified that commensal microbes facilitate accumulation of a monocyte population in neonatal skin, and that transient postnatal depletion of these monocytes led to heightened IL-17A production by skin T cells and exacerbated inflammatory skin pathologies. The authors found that neonatal skin monocytes were enriched in negative regulators of the IL-1 pathway and confirmed a key role for excessive IL-1R1 signaling in driving dysregulated type 17 inflammation. This article has no discernible connection to hirudotherapy, leech therapy, the leech secretome, or any related topic within ASH's domain. Caveat: No leeches or leech-derived compounds are involved; this study is entirely irrelevant to ASH's research library.

Citación

Commensal-myeloid crosstalk in neonatal skin regulates interleukin-1 signaling and cutaneous type 17 inflammation

Dhariwala MO et al. · Immunity, 2026

Contexto clínico relacionado

Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: June 18, 2026

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