CD55 organizes lipid raft-LCK signaling to potentiate NK-cell antitumor immunity.

CD55 on tumor-encountered NK cells organizes lipid raft–LCK signaling via CD97 engagement, and restoring CD55 boosts antitumor efficacy in vivo.

• Why it matters: NK cells rapidly lose function in the tumor microenvironment, and the mechanisms linking tumor encounter to sustained activating signaling are unclear.
• What they did: The study shows NK cells upregulate CD55 through an NKG2D–p65 transcriptional axis, then uses CD55–CD97 trans interactions to trigger lipid raft aggregation and LCK activation; it also tests CD55 restoration in conventional and CAR-engineered NK cells.
• The result: Prolonged tumor exposure progressively reduces CD55, impairing NK-cell function in the TME, while low CD55 in tumor-infiltrating NK cells correlates with poor clinical outcomes; reintroducing CD55 augments LCK signaling, effector function, persistence, and in vivo antitumor efficacy.

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