可溶性血管内皮生长因子1、AT1-AA与子痫前期

子痫前期的病理机制目前仍未完全清楚。子痫前期患者体内高水平的可溶性血管内皮生长因子1（sFlt-1）直接损伤血管内皮细胞,阻断血管生长,引起临床症状,可作为预测指标。抗血管紧张素Ⅱ1型受体自身抗体（ATI—AA）通过与受体结合,引起受体结构改变,产生病理性的细胞内信号,引起子痫前期。sFlt-1过量表达和AT1-AA的产生可能存在相关性,二者互相影响,共同参与子痫前期的病理生理过程。     

Loss of anti-AT1R reactivity in ELISA post-adsorption – False reactivity or interference in the assay?

Autoantibodies to Angiotensin II type 1 receptor (AT1R) are associated with detrimental outcomes in organ transplants. However, reports showed that adsorption with latex beads reduced positive anti-AT1R antibodies, suggesting possible false reactivity. To investigate this conundrum, we studied 11 samples positive for AT1R antibodies with an ELISA kit before and after adsorption. Adsorption significantly reduced the measurable level of AT1R antibodies (28.3 ± 9.8 vs. 6.3 ± 3.0 U/ml, p < 0.001). AT1R antibodies were lower when post-adsorption serum was added back at 1:1 ratio to the neat serum compared to the diluent control (8.6 ± 4.2 vs. 18.1 ± 10.3 U/ml, p = 0.02). Sham adsorption with the buffer from Adsorb Out™ kit without beads also suppressed the detection of anti-AT1R antibodies (32.7 ± 9.1 vs. 8.1 ± 3.9 U/ml, p < 0.001). Thus, rather than actively removing nonspecific antibodies by the beads, the adsorption process introduces soluble factors that interfere with the detection of anti-AT1R antibodies with the ELISA kit.