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DNAM-1–CD155 ligand-density-dependent NK cell activation

Candidate: concept label1 source documents6 linked claims
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Extracted Explainers

What the tool is doing

This paper-level concept describes how different densities of DNAM-1 ligands on target cells produce divergent NK-cell responses. Low CD155 or CD112 engagement is associated with stronger IFN-γ responses, whereas stronger CD155 engagement is associated with rapid DNAM-1 loss without added effector gain.

Source 1DOIPubMed

Resources required

The abstract indicates a need for target cells expressing low or high levels of CD155 or CD112 and assays that measure NK-cell activation and receptor surface expression.

Source 1DOIPubMed

What problem it solves

It helps explain an apparent paradox in which CD155 is a DNAM-1 ligand that can support activation, yet high CD155 expression is associated with poor prognosis and blunted NK benefit.

Source 1DOIPubMed

What it does not solve

The abstract does not establish the precise biochemical mechanism of DNAM-1 loss or define exact ligand-density cutoffs.

Source 1DOIPubMed

Alternatives

The abstract contrasts DNAM-1-dependent effects with TIGIT-focused interpretations by noting that TIGIT gene editing had no significant impact on target recognition in this setting.

Source 1DOIPubMed

Evidence Snippets

To assess the impact of ligand density on NK cell function, recognition of target cells expressing low and high levels of CD155 was compared.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1dependencysupports2026Source 1DOIPubMed

The improved activation induced by low levels of CD155 is still mediated through DNAM-1, as shown by selective disruption of the interaction.

Claim 2functional effectsupports2026Source 1DOIPubMed

Low levels of CD155 on target cells augment NK cell activation, most evident as elevated IFN-γ responses.

Claim 3functional effectsupports2026Source 1DOIPubMed

Recognition of target cells expressing CD112 results in modest DNAM-1 loss and heightened IFN-γ responses.

Claim 4mechanistic effectsupports2026Source 1DOIPubMed

High levels of CD155 also drive TIGIT loss from the NK cell surface, but TIGIT gene editing in primary NK cells has no significant impact on target cell recognition.

Claim 5mechanistic effectsupports2026Source 1DOIPubMed

High levels of CD155 drive rapid activation-induced downregulation of DNAM-1 on NK cells without enhancing IFN-γ responses.

Claim 6modelsupports2026Source 1DOIPubMed

DNAM-1 recognition of its ligands is poised such that low-avidity engagement augments NK-cell activation, whereas stronger engagement causes rapid DNAM-1 downregulation without significant enhancement of effector responses.