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Intravascular immune surveillance against viremia requires spatiotemporal coordination between Kupffer cells and ILC1s

Zhang et al. reveal that hepatic ILC1s rapidly transition from intravascular patrolling to motility arrest upon encountering infected Kupffer cells (KCs) during viremia. This behavioral switch, driven by cell intrinsic type I IFN signaling and coupled to ILC1 activation, fortifies the antiviral function of KCs to restrict systemic viral dissemination.

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