The IL-17-producing γδT cells (γδT17) have been attracting much attention because of their proinflammatory potential and contribution to various pathophysiological conditions. Although it is known that γδT17 develops in the fetal thymus, it remains largely unclear how γδT17 development is regulated by γδTCR signaling in γδT precursor cells. Here we show that hitherto unspecified γδTCR signaling pathway controls γδT17 development using knockout mice deficient in various key components of the proximal γδTCR signaling machinery. The mice deficient in a critical component of γδTCR signaling exhibited a complete loss of thymic γδT17 and an amelioration in psoriasis-like skin inflammation. These results indicate that the linage-specific TCR signal transduction contributes to the development of γδT17 and inflammatory responses.