IgA nephropathy is the most common primary GN worldwide. Previous research demonstrated that collectin11, an initiator of the complement lectin pathway, was involved in both AKI and chronic tubulointerstitial fibrosis. Here, we investigated the potential role of collectin11 in the pathogenesis of IgA nephropathy.

The deposition of collectin11 and other complement proteins was detected in glomeruli of 60 participants with IgA nephropathy by immunofluorescence. In vitro, human mesangial cells were treated with IgA1-containing immune complexes derived from participants with IgA nephropathy. Then, the expression of collectin11 in mesangial cells was examined by quantitative RT-PCR and immunofluorescence. The codeposition of collectin11 with IgA1 or C3 on mesangial cells was detected by immunofluorescence and proximity ligation assays.

In total, 37% of participants with IgA nephropathy (22 of 60) showed codeposition of collectin11 with IgA in the glomerular mesangium. Using an injury model of mesangial cells, we demonstrated that IgA1-immune complexes derived from participants with IgA nephropathy increased the secretion of collectin11 in mesangial cells with the subsequent deposition of collectin11 on the cell surface via the interaction with deposited IgA1-immune complexes. In vitro, we found that collectin11 bound to IgA1-immune complexes in a dose-dependent but calcium-independent manner. Furthermore, deposited collectin11 initiated the activation of complement and accelerated the deposition of C3 on mesangial cells.

In situ–produced collectin11 by mesangial cells might play an essential role in kidney injury in a subset of patients with IgA nephropathy through the induction of complement activation.

IgA 肾病是全世界最常见的原发性 GN。先前的研究表明，补体凝集素途径的启动子 collectin11 参与 AKI 和慢性肾小管间质纤维化。在这里，我们调查了 collectin11 在 IgA 肾病发病机制中的潜在作用。

通过免疫荧光法在 60 名 IgA 肾病参与者的肾小球中检测到 collectin11 和其他补体蛋白的沉积。在体外，人类系膜细胞用来自 IgA 肾病参与者的含有 IgA1 的免疫复合物进行处理。然后，通过定量RT-PCR和免疫荧光检查系膜细胞中collectin11的表达。collectin11 与 IgA1 或 C3 在肾小球系膜细胞上的共沉积通过免疫荧光和邻近连接测定法检测。

总共有 37% 的 IgA 肾病参与者（60 人中的 22 人）显示肾小球系膜中聚集素 11 与 IgA 共沉积。使用系膜细胞损伤模型，我们证明来自 IgA 肾病参与者的 IgA1 免疫复合物增加了系膜细胞中 collectin11 的分泌，随后 collectin11通过与沉积的 IgA1 免疫复合物相互作用沉积在细胞表面。在体外，我们发现 collectin11 以剂量依赖但不依赖钙的方式与 IgA1 免疫复合物结合。此外，沉积的 collectin11 启动了补体的激活并加速了 C3 在系膜细胞上的沉积。

系膜细胞原位产生的聚集素 11 可能通过诱导补体激活在 IgA 肾病患者亚群的肾损伤中发挥重要作用。