ArticleThe Journal of clinical investigation2025
Keratinocyte-neutrophil interactions revealed as targetable drivers of sustained inflammation in Sweet syndrome.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Neutrophils are key drivers of inflammation in Sweet syndrome (SS), a rare inflammatory skin disorder, but how they remain persistently activated in SS skin lesions has been unclear. In this issue of the JCI, Huang, Sati, and colleagues applied single-cell RNA-Seq and immunofluorescence to identify a subset of neutrophils in SS skin that display antigen-presenting cell-like (APC-like) features. The authors showed that when neutrophils interacted with keratinocytes, their lifespan was markedly extended, and they expressed MHC class II via activation of the serum amyloid A1/formyl peptide receptor 2 (SAA1/FPR2) signaling pathway. This, in turn, enabled T cell activation and sustained self-perpetuating inflammatory loops. These findings reveal a previously unrecognized keratinocyte-neutrophil circuit in SS and point to the SAA1/FPR2 axis as a potential target for more precise, mechanism-based therapy.
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