Interleukin‐17A (IL‐17A) is a pro‐inflammatory cytokine that has an important role at mucosal sites in a wide range of immune responses including infection, allergy and auto‐immunity. γδ T cells are recognized as IL‐17 producers, but based on the level of CD3 expression, we now define the remarkable ability of a CD3^bright γδ T‐cell subset with an effector memory phenotype to rapidly produce IL‐17A, but not interferon‐γ. CD3^bright γδ T cells uniformly express the canonical germline encoded Vγ6/Vδ1⁺ T‐cell receptor. They are widely distributed with a preferential representation in the lungs and skin are negatively impacted in the absence of retinoic acid receptor‐related orphan receptor gammat expression or endogenous flora. This population responded rapidly to various stimuli in a mechanism involving IL‐23 and NOD‐like receptor family, pyrin domain containing 3 (NLRP3)‐inflammasome‐dependent IL‐1β. Finally, we demonstrated that IL‐17‐producing CD3^bright γδ T cells responded promptly and strongly to pneumococcal infection and during skin inflammation. Here, we propose a new way to specifically analyze IL‐17‐producing Vγ6/Vδ1⁺ T cells based on the level of CD3 signals. Using this gating strategy, our data reinforce the crucial role of this γδ T‐cell subset in respiratory and skin disorders.