γδ T cell-derived IL-17A aggravates experimental epidermolysis bullosa acquisita in response to IL-1β

Neutralizing IL-17A in antibody transfer-induced epidermolysis bullosa acquisita mice ameliorates skin lesions, showing IL-17A promotes disease development in this model.

• Why it matters: IL-17A is linked to inflammatory signaling that recruits and activates neutrophils, but its specific contribution to experimental EBA remained unclear.
• What they did: In antibody transfer-induced EBA, gamma-delta T cells were the predominant IL-17A source, with reduced disease in gamma-delta TCR-deficient mice; IL-1β, not IL-23, drove IL-17A production in vitro and IL-1R deficiency markedly attenuated disease.
• The result: These findings support a previously unrecognized IL-1β/gamma-delta T cell/IL-17A axis that expands understanding of EBA immunopathogenesis in mice.

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