The control of influenza virus infections remains a global health problem due to the genetic variations within the virus that lead to the perpetual emergence of new strains. Annual vaccine strategies are aimed to boost antibody responses whereby influenza-specific antibody-secreting plasmablasts peak at day 7 post-vaccination. An increase in circulating T follicular helper (Tfh) cells has recently been correlated with the rise in plasmablasts and influenza-specific antibody titres in response to influenza vaccination. Tfh cells are essential for the generation of high-affinity memory B cells in germinal centers yet little is known about their role in the periphery. Our aim was to dissect the molecular nature of peripheral blood Tfh cells elicited after both influenza virus immunization and infection. The protective antibody titres (>40) were observed in 50% of individuals vaccinated with the 2014 Fluvax®. An increase in plasmablast and Tfh frequencies was detected on day 7 after immunization, followed by a decline on day 14. To understand TCR selection and stability of the influenza-responsive CXCR5+CXCR3+ICOS+PD-1+ Tfh population following influenza vaccination, we single-cell sorted Tfh and subsequently performed a single-cell multiplex paired TCRab repertoire. Our analysis revealed that while highly diverse TCR profiles were found in both a responder and a non-responder, a high proportion of identical TCRa chains (50%) were detected in both the overall CD4+CXCR5+ population and the Tfh sub-population in the non-responder only. This suggests an expansion or recruitment of distinct CDRa chains in the responder Tfh population. Current studies aim to understand the dynamics and TCR signatures of blood Tfh and plasmablasts in hospitalised influenza-infected patients. TCR repertoire dynamics of circulating Tfh cells in response to influenza vaccination or during acute influenza infection provide insights into how these cells are recruited in the periphery, their clonal stability and their role in providing effective influenza-specific antibody responses.