Upon encounter with their cognate antigen, B cells become activated, proliferate, undergo immunoglobulin class switch recombination (CSR), and differentiate into antibody-secreting cells. This process can either be direct, generating short-lived, proliferating plasmablasts, or the activated B cells can be rerouted into the germinal center (GC); transient structures in secondary lymphoid organs (SLOs) where B-cell clones undergo somatic hypermutation and are selected based on their B-cell receptor affinity to their specific antigen [1]. The outputs of GCs are both memory B cells and PCs. PCs are generally nondividing cells and have the capacity to secrete huge amounts of antibody for extended periods, thus providing the protective immunity associated with successful vaccines or naturally acquired immunity [2]. The parameters influencing the longevity of PCs have been the subject of a great deal of research and are thought to include both extrinsic and cell-intrinsic factors [3].

It has long been apparent that there is significant diversity in humoral immunity beyond the canonical response. Sources of diversity include the sites of initial immune challenge, the type of stimuli received, as well as the anatomical location in which the PCs reside. These factors in turn influence the lifespan of the PCs and require their adaptation to the tissue of residence. In this review, we will focus on the recent findings that begin to delineate the diversity of tissue PCs, the impact of this diversity on humoral immunity, and the factors influencing the longevity of the protection.