Institute of Medical Microbiology and Hygiene, Division of Immunology, University of Freiburg, Germany.
Eur J Immunol. 2010 May;40(5):1303-14. doi: 10.1002/eji.200939771.
The killer cell lectin-like receptor G1 (KLRG1) is expressed by NK and T-cell subsets and recognizes members of the classical cadherin family. KLRG1 is widely used as a lymphocyte differentiation marker in both humans and mice but the physiological role of KLRG1 in vivo is still unclear. Here, we generated KLRG1-deficient mice by homologous recombination and used several infection models for their characterization. The results revealed that KLRG1 deficiency did not affect development and function of NK cells examined under various conditions. KLRG1 was also dispensable for normal CD8+ T-cell differentiation and function after viral infections. Thus, KLRG1 is a marker for distinct NK and T-cell differentiation stages but it does not play a deterministic role in the generation and functional characteristics of these lymphocyte subsets. In addition, we demonstrate that E-cadherin expressed by K562 target cells inhibited NK-cell reactivity in transgenic mice over-expressing KLRG1 but not in KLRG1-deficient or WT mice. Hence, the inhibitory potential of KLRG1 in mice is rather weak and strong activation signals during viral infections may override the inhibitory signal in vivo.
杀伤细胞凝集素样受体 G1（KLRG1）表达于 NK 和 T 细胞亚群，识别经典钙黏蛋白家族成员。KLRG1 广泛用作人类和小鼠中淋巴细胞分化标志物，但 KLRG1 在体内的生理作用仍不清楚。在此，我们通过同源重组生成了 KLRG1 缺陷型小鼠，并利用多种感染模型对其进行了特征描述。结果表明，KLRG1 缺陷并不影响各种条件下 NK 细胞的发育和功能。KLRG1 对于病毒感染后 CD8+ T 细胞的正常分化和功能也是可有可无的。因此，KLRG1 是 NK 和 T 细胞分化阶段的一个标志物，但它在这些淋巴细胞亚群的生成和功能特征中不起决定性作用。此外，我们证明 K562 靶细胞表达的 E-钙黏蛋白抑制了过表达 KLRG1 的转基因小鼠中的 NK 细胞反应，但对 KLRG1 缺陷型或 WT 小鼠没有抑制作用。因此，在小鼠中，KLRG1 的抑制潜能相当弱，病毒感染期间的强烈激活信号可能会在体内消除抑制信号。
