Almost all current vaccines protect via induction of long-term antibody responses that result from Germinal centre (GC) reactions. Within GCs, T follicular helper (TFH) cells provide B cells with survival and differentiation signals essential for B cell maturation into memory B cells and antibody-secreting plasma cells. Multiple cellular interactions and co-ordination of transcriptional and migratory cues are required for the generation of dynamic GC reactions. During TFH differentiation, Bcl6 is upregulated following cognate dendritic cell interactions and this expression is reinforced via interactions with B cells at the T-B border. Bcl6 acts via multiple mechanisms to functionally activate TFH signature genes and repress other T helper (TH) fates, such as inhibition of T-bet (encoded by Tbx21), which is the lineage-specifying transcription factor of TH1 cells. Despite Bcl6-mediated repression, we found T-bet is highly expressed in both TFH and GC B cells, following influenza infection. Bcl6:T-bet complexes inhibit Bcl6 DNA binding, however, how this influences the individual functions of TFH and GC B cells to establish immune protection is incompletely understood. Using conditional T-bet-deficient animals, this study determines how T-bet controls the individual cell compartments (T and B cells) within dynamic GC reactions following influenza infection. Further, we demonstrate that T-bet is essential for the expression of the chemokine receptor CXCR3 within TFH and GC B cells. The role of CXCR3+ TFH is controversial, as studies have correlated their generation with either protective or non-protective B cell responses following infection and vaccination. We investigate the role of this down-stream effector and its ligands in the organisation of dynamic GC reactions.