Mast Cells and Innate Lymphoid Cells: Underappreciated Players in CNS Autoimmune Demyelinating Disease.
Mast Cells and Innate Lymphoid Cells: Underappreciated Players in CNS Autoimmune Demyelinating Disease.
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DOI：
10.3389/fimmu.2018.00514
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发表时间：
2018
影响因子：
7.3
通讯作者：
Weinberg RB
中科院分区：
文献类型：
--
作者：
Brown MA;Weinberg RB
多发性硬化症（MS）及其小鼠模型，实验性自身免疫性脑脊髓炎，是一种自身免疫性中枢神经系统炎症性疾病。由于受影响个体相对不可渗透的血脑屏障 (BBB) 的破坏，髓磷脂特异性 CD4+ 和 CD8+ T 细胞进入免疫特权中枢神经系统，并引发髓磷脂、少突胶质细胞和神经轴突破坏。然而，尽管对 T 细胞有绝对的需求，但越来越多的证据表明先天免疫细胞在疾病发病机制中也发挥着关键的放大作用。通过调节髓磷脂反应性 T 细胞反应的特征和强度并调节 BBB 完整性，先天细胞影响疾病的发生和进展。两类先天细胞，肥大细胞和先天淋巴细胞（ILC），在过敏和胃肠道炎症疾病模型中得到了最好的研究。然而，有新的证据表明这些细胞类型也对中枢神经系统炎症性疾病产生深远的影响。这两种细胞类型都居住在脑膜内，并且可以在疾病早期被激活，表达多种缓解疾病的细胞因子和趋化因子。在这篇综述中，我们讨论了肥大细胞和 ILC 如何对 MS 和其他 CNS 炎症性疾病产生疾病促进或保护作用，以及性激素如何影响这一结果。这些观察结果表明，可以在治疗上利用针对这些细胞及其独特介质的治疗。
Multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis, are autoimmune CNS inflammatory diseases. As a result of a breakdown in the relatively impermeable blood–brain barrier (BBB) in affected individuals, myelin-specific CD4+ and CD8+ T cells gain entry into the immune privileged CNS and initiate myelin, oligodendrocyte, and nerve axon destruction. However, despite the absolute requirement for T cells, there is increasing evidence that innate immune cells also play critical amplifying roles in disease pathogenesis. By modulating the character and magnitude of the myelin-reactive T cell response and regulating BBB integrity, innate cells affect both disease initiation and progression. Two classes of innate cells, mast cells and innate lymphoid cells (ILCs), have been best studied in models of allergic and gastrointestinal inflammatory diseases. Yet, there is emerging evidence that these cell types also exert a profound influence in CNS inflammatory disease. Both cell types are residents within the meninges and can be activated early in disease to express a wide variety of disease-modifying cytokines and chemokines. In this review, we discuss how mast cells and ILCs can have either disease-promoting or -protecting effects on MS and other CNS inflammatory diseases and how sex hormones may influence this outcome. These observations suggest that targeting these cells and their unique mediators can be exploited therapeutically.
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