In this thesis, we aim to further define the protective role of B cells during <italic>Salmonella</italic> infection. Understanding how B cells contribute to protective immunity is essential for designing more efficacious next generation vaccines against Typhoid and new vaccines against Paratyphoid and Non-Typhoid <italic>Salmonella</italic> strains. In the second chapter we test the hypothesis that systemic IgG production is an essential mechanism by which B cells protect against virulent infection. Surprisingly, we found that unlike B cells deficient mice, mice that lack the ability to secrete IgG or all antibodies are still largely protected from virulent <italic>Salmonella</italic> following resolution of infection with a vaccine strain. We further show that B cells, in the absence of antibody, are required for establishing robust memory Th1 responses. That B cells are important for protective immunity during secondary infection, suggests that we should better understand how this protection develops during a primary infection. In the third chapter, we aimed to define the kinetics and characteristics of the primary endogenous ovalbumin-specific B cell response during live vaccination with attenuated <italic>Salmonella</italic> expressing ovalbumin and OVA-specific B cell tetramers. We show that unlike immunization with OVA and adjuvant alone, there was a delay in the OVA-specific B cell responses until the infection had cleared. Additionally, we observed a delay in germinal center formation in these OVA-specific B cells, also in contrast to immunization with OVA and adjuvant alone. Upon co-administration of OVA with <italic>Salmonella</italic> infection, there was a decrease in the expansion and germinal center formation of OVA-specific B cells compared to mice that received OVA alone. We further discovered that, unlike culling of T cells during <italic>Salmonella</italic> infection, this inhibition of the B cell might not only be linked to expression of <italic>Salmonella</italic> Pathogenicity Island II proteins, but to effectors that modify the intraphagosomal load of bacteria.