The parasitic gastrointestinal nematode Nippostrongylus brasiliensis induces massive expansion of T helper type 2 (Th2) cells in the lung and small intestine. Th2 cells are a major source of interleukin‐4 and interleukin‐13, two cytokines that appear essential for rapid worm expulsion. It is unclear whether all Th2 cells induced during infection are pathogen‐specific because Th2 cells might also be induced by parasite‐derived superantigens or cytokine‐mediated bystander activation. Bystander Th2 polarization could explain the largely unspecific B‐cell response during primary infection. Furthermore, it is not known whether protective immunity depends on a polyclonal repertoire of T‐cell receptor (TCR) specificities. To address these unresolved issues, we performed adoptive transfer experiments and analysed the TCR‐Vβ repertoire before and after infection of mice with the helminth N. brasiliensis. The results demonstrate that all Th2 cells were generated by antigen‐specific rather than superantigen‐driven or cytokine‐driven activation. Furthermore, we show that worm expulsion was impaired in mice with a limited repertoire of TCR specificities, indicating that a polyclonal T‐cell response is required for protective immunity.