Early-life immune responses have been described as suboptimal, with neonates and infants being susceptible to infections. Vγ9Vδ2 T cells are the first T lymphocytes to be generated in the human fetus. Their T cell receptor-mediated responses to in vitro stimulation and their effector functions at birth are weaker compared with those in adults, possibly reflecting the need for tolerance in utero. However, here we show that upon transition to the prominent microbial exposure early after birth, public fetal-derived Vγ9Vδ2 T cells expand and differentiate into potent cytotoxic effector cells. Thus, they provide newborns with a first line of antimicrobial effector T cells in order to combat infections in early life.