When these anti-glycan IgG antibodies bind to abnormal IgA1, immune complexes are formed.

当这些抗糖基化的IgG抗体与异常IgA1结合，形成免疫复合物。

These immune complexes can travel through the bloodstream where they get trapped at sites of filtration, like the kidney.

这些免疫复合物可以通过血液循环，直到卡在某个地方，比如像肾这样的滤过场所。

Well, ultimately this damage is caused by immune complexes —complexes composed of an antigen with an antibody bound to it.

根本上来说，这种损伤是由免疫复合物引起的；复合物由抗原和抗体结合形成。

Immune complexes, though, might also form outside of the kidney, and then get carried through the bloodstream to the glomerulus and deposit in the basement membrane.

免疫复合物也能来自肾外，从血液循环中流入肾小球，并沉积在基底膜上。

The immune complexes specifically deposit in the mesangium which is the tissue in the Bowman's capsule that offers structural support to the glomerular capillaries.

这些免疫复合物常常沉积在肾小球系膜；肾小球系膜是Bowman囊的一部分，为肾小球血管球提供结构支持。

In these sorts of infections, IgA1 antibody production gets ramped up, leading to IgG anti-glycan formation, and immune complex deposition in the glomerular mesangium, causing inflammation.

在这些感染情况下，IgA1抗体产生增多，导致抗糖基化的抗体IgG形成，免疫复合物便沉积在肾小球系膜，产生炎症反应。

IgA nephropathy is therefore a type III hypersensitivity disorder, meaning that pathology and inflammation will happen at the site the immune complexes deposit, not where they are formed.

因此IgA肾病是一种III型超敏反应，意味着病理和炎症反应会发生在免疫复合物沉积的地方，而不是发生在免疫复合物形成的地方。

Over time, as a reaction to the immune deposits, GBM matrix is deposited in between the immune complexes, which makes the GBM appear thickened on histology.

随着免疫复合物日趋沉积，肾小球基膜基质间布满了免疫复合物，使肾小球基膜在组织学上表现为增厚。

Those immune complexes can also be visualized on immunofluorescence, although one important finding that can help differentiate from other immune-complex mediated nephropathies is that these complexes involve IgA.

用免疫荧光电镜也可以看到这些免疫复合物，但有一点需要注意，有助于和其他免疫复合物介导的肾病区分，就是这些免疫复合物包含IgA。

On light microscopy, there'll often be mesangial proliferation, or expansion of the mesangium, and upon getting a closer look with electron microscopy, there'll be immune complexes deposited within the mesangium.

光学显微镜下，常常可见系膜增生或系膜扩张，进一步电镜下观察，可见免疫复合物沉积于系膜上。

Alright, quick recap—membranous glomerulonephritis is where immune complexes deposit in the GBM, causing a thickening of that GBM and a " spike and dome" appearance that leads to nephrotic syndrome.

好，快速回顾一下：在膜性肾小球肾炎中，免疫复合物沉积在肾小球基膜，引起肾小球基膜增厚和“钉状突起”，导致肾病综合征。

Whether they bind directly to the GBM, or come from somewhere else, these immune complexes are called subepithelial deposits because they're sandwiched right between the epithelial cells or podocytes, and the GBM.

无论是直接与肾小球基膜结合或从别处而来，这些免疫复合物称之为上皮下沉积物，因为它们位于足细胞这类上皮细胞和肾小球基膜之间。

When the abnormal IgA1-IgG immune complexes deposit in the mesangium, the alternative complement pathway is activated, leading to the release of proinflammatory cytokines and migration of macrophages into the kidney, all of which contributes to glomerular injury.

当异常的IgA1-IgG免疫复合物沉积在系膜上时，补体旁路途径被激活，导致促炎因子的释放，同时促进巨噬细胞向肾迁移，以上所有反应会导致肾小球的损伤。

One potential circulating antigen that's been identified is cationic bovine serum albumin, which is present in cow's milk and beef protein, and can escape the intestinal barrier, cause immune complex formation, and deposit in the GBM.

一种已发现的潜在循环抗原是阳离子化牛血清白蛋白，存在牛奶和牛肉蛋白质中，并可逃离肠道屏障，导致免疫复合物形成，沉积在基底膜。