T cell–dependent germinal center (GC) reactions are the pinnacle of adaptive immune responses, with profound effects on human health and disease. It has long been known that ligands of an innate immune pattern recognition receptor subgroup, TLRs, amplify antibody responses; however, the mechanisms regulating this phenomenon are poorly understood. In this issue of the JCI, Raso et al. demonstrate that αvβ3 integrins regulate the magnitude and speed of TLR-augmented GC reactions, limiting both short- and long-term humoral immunity. This phenomenon is dependent on a noncanonical form of the autophagy pathway and Rubicon, a noncanonical autophagy-associated protein. B cell–specific deletion of the gene encoding αvβ3 integrin enhanced GC responses in mice and conferred a dramatic survival advantage compared with controls after influenza infection, confirming that B cell integrin manipulation represents a potential and exciting target for augmenting or inhibiting GC reactions.
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