The mechanisms that drive impaired immunity in people with kidney disease remain unclear. A study by Partha Biswas and colleagues now links a uraemic toxin to defective germinal centre (GC) B cell responses in mice.

Gene-expression analysis and cell staining suggested reduced proliferation and increased apoptosis in GC B cells from KD mice compared with controls. In vitro, exposing plasmablasts to uraemic toxins at concentrations observed in people with advanced KD revealed that hippuric acid, which can bind to GPR109A (encoded by Niacr1), increased plasmablast apoptosis. The researchers showed that the GC response defect observed in animals with KD was dependent on the presence of GPR109A, as Niacr1^–/– animals with AA-induced KD still had a normal GC response. Moreover, when B cell-deficient mice received Niacr1^–/– B cells, induction of KD with AA did not compromise the number of NP-specific B cells detected after immunization.

导致肾病患者免疫力受损的机制仍不清楚。Partha Biswas 及其同事的一项研究现在将尿毒症毒素与小鼠的生发中心 （GC） B 细胞反应缺陷联系起来。

基因表达分析和细胞染色表明，与对照组相比，KD 小鼠 GC B 细胞的增殖减少和凋亡增加。在体外，将浆母细胞暴露于在晚期 KD 患者中观察到的浓度的尿毒症毒素中，发现可与 GPR109A 结合（由 Niacr1 编码）的马尿酸增加了浆母细胞细胞凋亡。研究人员表明，在 KD 动物中观察到的 GC 反应缺陷取决于 GPR109A 的存在，因为 AA 诱导的 KD 的 Niacr1^–/– 动物仍然具有正常的 GC 反应。此外，当 B 细胞缺陷小鼠接受 Niacr1^–/– B 细胞时，AA 诱导 KD 不会影响免疫后检测到的 NP 特异性 B 细胞的数量。