T 细胞缺陷并不会减少 NMO-IgG 和补体脑内注射引起的小鼠病变。

T cell deficiency does not reduce lesions in mice produced by intracerebral injection of NMO-IgG and complement.

机构信息

Academic Neurosurgery Unit, St. George's, University of London, London SW170RE, UK.

出版信息

J Neuroimmunol. 2011 Jun;235(1-2):27-32. doi: 10.1016/j.jneuroim.2011.03.007. Epub 2011 Apr 13.

DOI:10.1016/j.jneuroim.2011.03.007

Abstract

We reported recently that intracerebral administration of NMO-IgG with human complement produces neuromyelitis optica (NMO) lesions in mice. We examined the role of T cells in the formation of NMO lesions by comparing brain histopathology in wildtype and nude mice. Brains were co-injected with IgG from NMO patients and human complement. At 24h and 5days, wildtype vs. nude mouse brains had comparable inflammation (CD45 immunoreactivity), loss of myelin (Luxol Fast Blue staining) and loss of AQP4 immunoreactivity. We conclude that T cells are not required for the formation of NMO lesions in this mouse model.

摘要

我们最近报道称，脑内给予含有人类补体的 NMO-IgG 可在小鼠中产生视神经脊髓炎（NMO）病变。我们通过比较野生型和裸鼠的脑组织病理学来研究 T 细胞在 NMO 病变形成中的作用。脑内共同注射来自 NMO 患者的 IgG 和人类补体。在 24 小时和 5 天时，野生型与裸鼠的大脑具有相似的炎症（CD45 免疫反应性）、髓鞘丢失（卢索快速蓝染色）和 AQP4 免疫反应性丧失。我们得出结论，在这种小鼠模型中，T 细胞不是 NMO 病变形成所必需的。