The functional dichotomy of Vδ1+ (mucosal-resident) and Vδ2+ (blood-circulating) γδ T cells dictates their distinct contributions to post-stroke neuroinflammation: Vδ2+ cells dominate early Interleukin-17 (IL-17)-driven neutrophil recruitment, while it is assumed that Vδ1+ subsets may modulate late-stage repair via gut-derived metabolites (30, 31). This evidence concerns the gene IL17A and stroke disorder.