Influenza A virus causes morbidity and mortality to millions of people worldwide. Current vaccination strategies against influenza have focused on generating antibodies that are only capable of protecting against a single strain of influenza necessitating annual vaccination against the virus. Recent studies have highlighted the importance of CD8+ T cell-mediated immunity in generating cross-protective responses against influenza infection. This process, mainly dependent on cell-mediated immunological memory including the recently defined tissue resident memory CD8+ T cells, has become a focus on generating new vaccines against influenza. Hence understanding the optimal generation of effector T cells, specifically CD8+ T cells, in response to influenza can help provide better future vaccination designs. The chemokine receptor CCR6 has been implicated in generating effective T cell mucosal immunity. CCR6 is expressed by effector/memory T cells and by dendritic cells (DC), which respond to the ligand CCL20. Here, we investigated the role of CCR6 in generating CD8+ T cell responses to influenza. We show that CCR6-deficient mice produce fewer tissue resident memory CD8+ T cells and succumb to heterotypic rechallenge of influenza infection. We have determined that lung dendritic cells but not lung CD8+ T cells express CCR6. Assessment of in vivo migration of DCs from the lungs to the mediastinal lymph nodes (mLN) following influenza infections shows that CCR6 is required for late phase recruitment of DCs to the mLN. These data suggest that CCR6 controls DC migratory steps that is required for the generation of memory CD8+ T cells following influenza infections.