Experimental Immunology, University of Zurich, Zurich, Switzerland.
Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Göttingen, Germany.
Trends Neurosci. 2019 Oct;42(10):667-679. doi: 10.1016/j.tins.2019.07.008. Epub 2019 Aug 29.
Neuro-immune interactions are not only vital for the control of neurotropic pathogens, but also appear to influence brain development and homeostasis. During immune surveillance, T cells can patrol the CNS-associated border regions to sense pathogenic alterations. While access to the CNS parenchyma is restricted in the steady state, various disease processes can initiate parenchymal T cell CNS invasion. However, to breach the glia limitans, T cells must become reactivated within the meningeal spaces. T cells cannot sense native antigens (Ags), but instead recognize small processed peptides bound to MHC molecules and presented on the surface of Ag-presenting cells (APCs). In this review, we focus on (CD4) T cell-CNS interactions that are dependent on Ag recognition. We discuss the potential paths and mechanisms of T cell entry into the CNS, in particular with respect to CNS-resident APCs, which present CNS-derived Ag in the absence of inflammation.
神经免疫相互作用不仅对控制神经亲和病原体至关重要，而且似乎还影响大脑发育和稳态。在免疫监视过程中，T 细胞可以在中枢神经系统相关边界区域巡逻，以感知病原体的变化。虽然在稳定状态下，T 细胞进入中枢神经系统实质受到限制，但各种疾病过程都可以引发实质 T 细胞中枢神经系统浸润。然而，要突破神经胶质界限，T 细胞必须在脑膜空间内重新激活。T 细胞不能感知天然抗原 (Ags)，而是识别与 MHC 分子结合并在抗原呈递细胞 (APC)表面呈现的小处理肽。在这篇综述中，我们专注于依赖于 Ag 识别的 (CD4) T 细胞与中枢神经系统的相互作用。我们讨论了 T 细胞进入中枢神经系统的潜在途径和机制，特别是关于在没有炎症的情况下在中枢神经系统中呈现中枢神经系统衍生 Ag 的中枢神经系统驻留 APC。
