A fibroblast-CD8+ T cell circuit drives a Type 1 shift in allergic inflammatory memory

Repeated challenge in murine T2 atopic dermatitis–like inflammation drives a T2-to-T1 shift in recall, layering IFN signaling and cytotoxic recruitment onto amplified T2 responses.

• Why it matters: In barrier tissues, inflammatory memory can exaggerate recall, but it was unclear whether memory re-engages programs beyond the initiating inflammatory type.
• What they did: Using longitudinal single-cell RNA-sequencing in murine T2 and T17 models, the study found that CD8+ tissue-resident memory T cells expanded with repeated challenge and produced IFN-gamma, TNF, and IL-13, resembling treatment-refractory Trm cells in AD.
• The result: Fibroblast rewiring supported by Trm-derived T1 cytokines and IL-4-rich T2 milieu amplified allergic recall via IL-15 and CCL19, and the two-cell circuit’s T1 and T2 effector arms were conserved in human AD.

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