Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Eur J Immunol. 2011 Dec;41(12):3627-31. doi: 10.1002/eji.201141876. Epub 2011 Nov 10.
Nod2 belongs to the nucleotide-binding domain leucine-rich repeat family of proteins and senses bacterial cell wall components to initiate innate immune responses against various pathogens. Recently, it has been reported that T-cell-intrinsic expression of Nod2 promotes host defense against Toxoplasma gondii infection by inducing type 1 immunity. Here, we present results that demonstrate that Nod2 does not play a role in the defense against T. gondii infection. Nod2-deficient mice were fully capable of inducing Th1 immune responses and did not show enhanced susceptibility to infection. Upon TCR stimulation in vitro, Nod2-deficient CD4(+) T cells showed normal activation, IL-2 production, proliferation, and Th1/2 differentiation. Nod2 mRNA and protein were expressed in CD4(+) T and CD8(+) T cells at substantial levels. Therefore, Nod2, although expressed in CD4(+) T cells, does not have an intrinsic function in T-cell activation and differentiation.
Nod2 属于核苷酸结合结构域富含亮氨酸重复蛋白家族,能够感知细菌细胞壁成分,从而启动针对各种病原体的先天免疫反应。最近有报道称,Nod2 在 T 细胞中的内在表达通过诱导 I 型免疫促进宿主对弓形虫感染的防御。在这里,我们提供的结果表明,Nod2 并不参与防御弓形虫感染。Nod2 缺陷型小鼠完全能够诱导 Th1 免疫反应,并且对感染没有表现出易感性增加。在体外 TCR 刺激下,Nod2 缺陷型 CD4(+) T 细胞表现出正常的激活、IL-2 产生、增殖和 Th1/2 分化。Nod2 mRNA 和蛋白在 CD4(+) T 和 CD8(+) T 细胞中以相当高的水平表达。因此,Nod2 虽然在 CD4(+) T 细胞中表达,但在 T 细胞激活和分化中没有内在功能。