Although influenza vaccination reduces disease severity, it has limited impact on airborne transmission. Understanding how pre-existing immunity shapes viral replication and airborne shedding is essential to identify host factors that influence transmission.   We investigated how homologous and heterologous pre-existing immunity influences influenza A virus shedding kinetics in the ferret model. Using a state-of-the-art air-sampling setup, we quantified infectious airborne viruses expelled by ferrets with defined immune backgrounds. Prior immunity was established through vaccination (H1N1, H3N2, H1N2, or H3N1) or infection (H1N1 or H3N2) followed by challenge infection with H1N1. Air samples were collected alongside daily nasal and throat swabs, clinical assessments, and immunological assays (serology and T-cell analyses).   Ferrets homologously re-challenged following H1N1 infection had no detectable infectious virus in air samples and swabs, consistent with the pre-challenge immune response. Among the remaining groups, the total amount of airborne virus expelled did not differ significantly. Nasal viral replication—known to correlate with airborne transmission—was reduced following prior H3N2 infection and, to a lesser extent, following homologous vaccination, whereas heterologous vaccination had minimal impact. Ferret T-cell analysis revealed H1- and NP-specific responses only after challenge, highlighting that vaccination alone did not prime detectable cellular immunity.   Pre-existing immunity was found to differentially impact influenza A virus replication and airborne shedding. Natural infection, which more effectively induces mucosal immunity, restricted upper respiratory replication and reduced shedding, unlike parental immunization. This work identifies host immune history as a key determinant of influenza A virus transmission and informs strategies to limit influenza virus spread.