Moreover, NETs polarize macrophages toward the M1 phenotype, increasing their bactericidal capacity; induce dendritic cell maturation to promote antigen presentation; stimulate B cells to secrete B cell activating factor (BAFF), thereby bridging innate and adaptive immunity; and, via gasdermin-D pores, release IL-1β to recruit additional neutrophils to the site of infection [85,86]. This evidence concerns the gene TNFSF13B and infection.