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To the Editor TIGIT versus CD226: Hegemony or coexistence?

机译:编辑TIGIT与CD226:霸权或共存?

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In a recent paper published in the European Journal of Immunology, Stani-etsky et al. demonstrated that TIGIT inhibits the cytotoxicity of murine NK cells upon interaction with its counter-receptor CD 155 expressed by the target cells [1]. Interestingly, a subpopula-tion 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/CTIA-4 that share the same receptors of the B7 family [3-5].
机译:在最近的一篇论文发表在欧洲免疫学杂志》上,Stani-etsky et al。证明TIGIT抑制细胞毒性小鼠NK细胞的相互作用的counter-receptor CD 155所表达的目标细胞[1]。细胞不仅表达TIGIT CD226,另一个counter-receptor CD155。代表一个激活受体在细胞毒性T细胞和NK细胞[2]。令人信服地证明了表面等离子体共振,在鼠标很像人类,与亲和力高于TIGIT CD155结合CD226。结果非常让人想起研究对立的受体和配体配对和假设被提出的几组将CD155 / CD226 / TIGIT三配位开关功能的亲属关系系统,如CD28 / CTIA-4共享相同的B7家族的受体[3 - 5]。

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