Positionally distinct interferon stimulated dermal immune acting fibroblasts promote neutrophil recruitment in Sweet’s syndrome

Author:

Cavagnero Kellen J.ORCID,Albright Julie,Li Fengwu,Dokoshi Tatsuya,Bogle Rachael,Kirma Joseph,Kahlenberg J. Michelle,Billi Allison C.,Fox Jennifer,Coon Anthony,Dobry Craig J.,Hinds Brian,Tsoi Lam C.,Harms Paul W.,Gudjonsson Johann E.,Gallo Richard L.ORCID

Abstract

AbstractSweet’s syndrome is a poorly understood inflammatory skin disease characterized by neutrophil infiltration to the dermis. Single-nucleus and bulk transcriptomics of archival clinical samples of Sweet’s syndrome revealed a prominent interferon signature in Sweet’s syndrome skin that was reduced in tissue from other neutrophilic dermatoses. This signature was observed in different subsets of cells, including fibroblasts that expressed interferon-induced genes. Functionally, this response was supported by analysis of cultured primary human dermal fibroblasts that were observed to highly express neutrophil chemokines in response to activation by type I interferon. Furthermore, single-molecule resolution spatial transcriptomics of skin in Sweet’s syndrome identified positionally distinct immune acting fibroblasts that included a CXCL1+ subset proximal to neutrophils and a CXCL12+ subset distal to the neutrophilic infiltrate. This study defines the cellular landscape of neutrophilic dermatoses and suggests dermal immune acting fibroblasts play a role in the pathogenesis of Sweet’s syndrome through recognition of type I interferons.

Publisher

Cold Spring Harbor Laboratory

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