Carlyle J R, Martin A, Mehra A, Attisano L, Tsui F W, Zúñiga-Pflücker J C
Departments ofImmunology and Anatomy and Cell Biology, University of Toronto, Toronto, Ontario, Canada.
J Immunol. 1999 May 15;162(10):5917-23.
The mouse NK1.1 Ag originally defined as NK cell receptor (NKR)-P1C (CD161) mediates NK cell activation. Here, we show that another member of the mouse CD161 family, NKR-P1B, represents a novel NK1.1 Ag. In contrast to NKR-P1C, which functions as an activating receptor, NKR-P1B inhibits NK cell activation. Association of NKR-P1B with Src homology 2-containing protein tyrosine phosphatase-1 provides a molecular mechanism for this inhibition. The existence of these two NK1.1 Ags with opposite functions suggests a potential role for NKR-P1 molecules, such as those of the Ly-49 gene family, in regulating NK cell function.
最初被定义为自然杀伤(NK)细胞受体(NKR)-P1C(CD161)的小鼠NK1.1抗原介导NK细胞活化。在此,我们表明小鼠CD161家族的另一个成员NKR-P1B代表一种新型NK1.1抗原。与作为活化受体发挥作用的NKR-P1C不同,NKR-P1B抑制NK细胞活化。NKR-P1B与含Src同源2结构域的蛋白酪氨酸磷酸酶-1的结合为这种抑制作用提供了一种分子机制。这两种具有相反功能的NK1.1抗原的存在表明NKR-P1分子(如Ly-49基因家族的分子)在调节NK细胞功能方面具有潜在作用。