JAK1/2 Inhibition Restores Tissue Integrity by Rewiring Type 1/2 Immunity Toward Targetable IL-17 Responses

Topical JAK1/2 inhibition in a chronic, barrier-dysfunction skin inflammation model suppresses pathogenic CD8 T cells’ IFN-{gamma} while shifting CD4 T cells toward Th17, preserving IL-17A type 3 immunity.

• Why it matters: Chronic skin inflammation disrupts immune–epithelial coordination, driving progressive tissue destruction; the effects of JAK inhibition in this complex environment are not fully defined.
• What they did: The study used single-cell transcriptomics and functional profiling to analyze immune and epithelial changes after topical JAK1/2 blockade, including combination testing with IL-17A blockade.
• The result: JAK1/2 inhibition rapidly restores epithelial barrier integrity via tight junction reinforcement, recovers antimicrobial defenses, reduces bacterial burden, and combination JAK1/2 plus IL-17A blockade further improves tissue homeostasis by targeting residual IL-17A-mediated pathology.

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