Epithelial barriers are vital components of the innate immune system. This barrier is provided by tight junctions and compromised by proinflammatory cytokine signaling. Study of claudin 4 live-cell protein dynamics shows that tight junctions are self-assembling systems that undergo remodeling through heterotypic claudin incompatibility.
Junctional adhesion molecule-A (JAM-A) is a tight junction–associated signaling protein that homodimerizes across cells at a unique motif to activate the small GTPase Rap2, previously implicated in the regulation of barrier function. JAM-A may therefore act as a barrier-inducing molecular switch that is activated when cells become confluent.
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