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To the EditorTIGIT versus CD226: Hegemony or coexistence?

In a recent paper published in the European Journal of Immunology, Stanietsky et al. demonstrated that TIGIT inhibits the cytotoxicity of murine NK cells upon interaction with its counterreceptor CD155 expressed by the target cells [1]. Interestingly, a subpopulation of the cells not only expresses TIGIT but also CD226, another counter-receptor of CD155. CD226 represents an activating receptor on cytotoxic T cells and NK cells [2]. Stanietsky et al. [1] convincingly demonstrated by surface plasmon resonance that in mouse very much like in human, TIGIT binds to CD155 with higher affinity than CD226. As discussed by the authors, these findings are highly reminiscent of other well-studied antagonistic receptor/ligand pairings and a hypothesis was put forward by several groups placing the CD155/CD226/TIGIT triad in functional kinship to ligand switch systems such as CD28/CTLA-4 that share the same receptors of the B7 family [3–5]. Here, CTLA-4-mediated inhibition of T-cell activation becomes dominant soon after initial stimulation via CD28 because the activa-