This myelin is produced by oligodendrocytes, which are a group of cells that support neurons.

髓鞘由支持神经元的少突胶质细胞形成。

Unfortunately, though, over time as the oligodendrocytes die off the remyelination stops and the damage becomes irreversible with the loss of axons.

病情长期下去因为少突胶质细胞的死亡，髓鞘将停止再生，并且随着神经元轴索的减少，这些损伤不可逆。

Those B-cells begin to make antibodies that mark the myelin sheath proteins, and then the macrophages use those antibody markers to engulf and destroy the oligodendrocytes.

那些B淋巴细胞分泌抗体，标记于髓鞘蛋白上，巨噬细胞利用抗体标志吞噬摧毁少突胶质细胞。

Without oligodendrocytes, there's no myelin to cover the neurons, and this leaves behind areas of scar tissue, also called plaques or sclera.

没了少突胶质细胞，也就没有保护神经元的髓鞘，还会留下斑痕组织（硬化斑）。

Early on in multiple sclerosis, the oligodendrocytes will heal and extend out new myelin to cover the neurons, which is a process called remyelination.

多发性硬化早期，少突胶质细胞可以自我修复，形成新髓鞘包裹住神经元，叫作髓鞘再生。

In other words, an autoimmune attack on the oligodendrocytes might happen, and then regulatory T cells will come in to inhibit or calm down the other immune cells, leading to a reduction in the inflammation.

换个说法，自身免疫攻击少突胶质细胞后，T调节淋巴细胞会赶到并安抚其它免疫细胞，从而减轻炎症。

During a flare, T-cells cause inflammation and damage to oligodendrocytes in the central nervous system, which leaves behind scarred areas of demyelinated neurons called plaques, which causes a variety of symptoms depending on the location.

在发作期间，T淋巴细胞导致炎症并损伤中枢神经系统的少突胶质细胞，在脱髓鞘神经元处形成瘢痕（硬化斑），从而根据部位的不同产生不同的症状。

And this means that those myelin specific T-cells release cytokines like IL-1, IL-6, TNF-alpha, and interferon-gamma, and together dilate the blood vessels which allows more immune cells to get in, as well as directly cause damage to the oligodendrocytes.

髓鞘敏感的T淋巴细胞释放细胞因子，比如IL-1、IL-6、α-肿瘤坏死因子、γ-干扰素，一起扩张血管让更多免疫细胞进入，直接损伤少突胶质细胞。