Negative regulators that mediate ocular immune privilege.
Negative regulators that mediate ocular immune privilege.
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DOI：
10.1002/jlb.3mir0817-337r
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发表时间：
2018-02-12
影响因子：
5.5
通讯作者：
Ng TF
中科院分区：
文献类型：
--
作者：
Taylor AW;Ng TF
眼睛微环境已经适应了炎症的几种负调节剂，以维持免疫豁免和视轴的健康。眼内的几种组成性产生的负调节因子TGF-β2、α-黑素细胞刺激激素（α-MSH）、Fas配体（FasL）和PD-L1突出，因为它们能够影响多种炎症途径，并且它们是促进免疫耐受的一部分。这些调节剂证明了免疫豁免的能力，以防止炎症的活化，并抑制效应免疫细胞的活化，即使在由内毒素和自身免疫性疾病诱导的眼部炎症的条件下。此外，这些负调节因子促进和扩大介导调节性免疫和致耐受性免疫的免疫细胞。这反过来又使免疫细胞本身成为炎症的负调节剂。这提供了对免疫豁免的更好理解，因为它包括炎症的分子和细胞负调节因子。这将意味着，通过使用分子和细胞作为炎症的负调节因子，可以开发出治疗自身免疫性疾病的潜在新方法。
The ocular microenvironment has adapted several negative regulators of inflammation to maintain immune privilege and health of the visual axis. Several constitutively produced negative regulators within the eye TGF-β2, α-melanocyte stimulating hormone (α-MSH), Fas ligand (FasL), and PD-L1 standout because of their capacity to influence multiple pathways of inflammation, and that they are part of promoting immune tolerance. These regulators demonstrate the capacity of immune privilege to prevent the activation of inflammation, and to suppress activation of effector immune cells even under conditions of ocular inflammation induced by endotoxin and autoimmune disease. In addition, these negative regulators promote and expand immune cells that mediate regulatory and tolerogenic immunity. This in turn makes the immune cells themselves negative regulators of inflammation. This provides for a greater understanding of immune privilege in that it includes both molecular and cellular negative regulators of inflammation. This would mean that potentially new approaches to the treatment of autoimmune disease can be developed through the use of molecules and cells as negative regulators of inflammation.