The regulation of the CNS innate immune response is vital for the restoration of tissue homeostasis (repair) after acute brain injury: a brief review.
The regulation of the CNS innate immune response is vital for the restoration of tissue homeostasis (repair) after acute brain injury: a brief review.
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DOI：
10.4061/2010/151097
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发表时间：
2010-08-09
影响因子：
2
通讯作者：
Neal JW
中科院分区：
文献类型：
--
作者：
Griffiths MR;Gasque P;Neal JW
神经元和神经胶质细胞通过参与中枢神经系统先天免疫反应来应对急性损伤。这涉及识别和清除“非自我”病原体和“改变自我”的凋亡细胞。吞噬细胞受体（CD14、CD36、TLR-4）清除“非自身”病原体；神经元和神经胶质细胞表达“死亡信号”以启动 T 细胞凋亡。补体调理素 C1q、C3 和 iC3b 通过与 CR3 和 CR4 受体相互作用，促进凋亡细胞的清除。凋亡细胞也会被胶质细胞表达的清道夫受体 CD14、Prs-R、TREM 清除。神经胶质细胞表达的丝氨酸蛋白酶抑制剂还可以对抗损伤后进入中枢神经系统的凝血酶和其他全身蛋白的神经毒性作用。补体途径和 T 细胞激活均受到神经胶质细胞和神经元表达的补体调节蛋白的调节。 CD200 和 CD47 是神经元表达的 NIReg，作为“别吃我”信号，它们抑制小胶质细胞活性，防止宿主细胞攻击。神经干细胞调节 T 细胞活化、增加 Treg 群体并抑制促炎细胞因子表达。干细胞还与化学引诱剂 C3a、C5a、SDF-1 和凝血酶相互作用，促进干细胞迁移到受损组织中，以支持组织稳态。
Neurons and glia respond to acute injury by participating in the CNS innate immune response. This involves the recognition and clearance of “not self ” pathogens and “altered self ” apoptotic cells. Phagocytic receptors (CD14, CD36, TLR–4) clear “not self” pathogens; neurons and glia express “death signals” to initiate apoptosis in T cells.The complement opsonins C1q, C3, and iC3b facilitate the clearance of apoptotic cells by interacting with CR3 and CR4 receptors. Apoptotic cells are also cleared by the scavenger receptors CD14, Prs-R, TREM expressed by glia. Serpins also expressed by glia counter the neurotoxic effects of thrombin and other systemic proteins that gain entry to the CNS following injury. Complement pathway and T cell activation are both regulated by complement regulatory proteins expressed by glia and neurons. CD200 and CD47 are NIRegs expressed by neurons as “don't eat me” signals and they inhibit microglial activity preventing host cell attack. Neural stem cells regulate T cell activation, increase the Treg population, and suppress proinflammatory cytokine expression. Stem cells also interact with the chemoattractants C3a, C5a, SDF-1, and thrombin to promote stem cell migration into damaged tissue to support tissue homeostasis.