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首页> 外文期刊>Immunology and Cell Biology >Importance of carbohydrate in the interaction of Tamm-Horsfall protein with complement 1q and inhibition of classical complement activation.
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Importance of carbohydrate in the interaction of Tamm-Horsfall protein with complement 1q and inhibition of classical complement activation.

机译：碳水化合物在Tamm-Horsfall蛋白与补体1q相互作用和经典补体激活抑制中的重要性。

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摘要

Tamm-Horsfall protein (THP) binds strongly to complement 1q (C1q), a key component of the classical complement pathway. The goals of this study were to determine whether THP altered the activation of the classical complement pathway and whether the carbohydrate portion of THP was involved in this glycoprotein's binding to C1q and alteration of complement activation. The ability of THP to prevent complement activation in diluted serum or plasma incubated at 37 degrees C was assessed using both a haemolytic assay with antibody-sensitized sheep RBC and a C4d ELISA. Both these methods showed that THP inhibited activation of the classical complement pathway in a dose-dependent manner. Glycosidases were used to remove most of the carbohydrate from THP. This partially deglycosylated THP bound human IgG with a higher affinity (KD1 = 1.4 nmol/L; KD2 = 0.31 micromol/L) than did intact THP (KD1 = 33.4 nmol/L; KD2 31.0 micromol/L). An ELISA showed that removal of carbohydrate from THP reduced, but did not eliminate, the ability of this protein to inhibit binding of C1q to intact THP. Haemolysis assays using antibody-sensitized sheep RBC showed that removal of THP carbohydrate eliminated the ability of THP to protect against complement activation. In conclusion, THP inhibited the activation of the classical complement pathway that occurred in diluted serum or plasma. The carbohydrate moieties of THP appeared to be important in this inhibitory activity.
机译：Tamm-Horsfall蛋白（THP）与补体1q（C1q）牢固结合，补体1q是经典补体途径的关键组成部分。这项研究的目的是确定THP是否改变了经典补体途径的激活，以及THP的碳水化合物部分是否参与了这种糖蛋白与C1q的结合以及补体激活的改变。使用具有抗体致敏羊RBC的溶血测定法和C4d ELISA评估了THP防止在37°C孵育的稀释血清或血浆中补体激活的能力。这两种方法均显示THP以剂量依赖性方式抑制经典补体途径的激活。糖苷酶用于从THP中去除大部分碳水化合物。与完整的THP（KD1 = 33.4 nmol / L; KD2 31.0 micromol / L）相比，这种部分去糖基化的THP结合的人IgG具有更高的亲和力（KD1 = 1.4 nmol / L; KD2 = 0.31 micromol / L）。 ELISA显示，从THP中除去碳水化合物可降低但不能消除该蛋白抑制C1q与完整THP结合的能力。使用抗体致敏羊RBC进行的溶血分析表明，去除THP碳水化合物消除了THP防御补体激活的能力。总之，THP抑制了稀释血清或血浆中经典补体途径的激活。 THP的碳水化合物部分似乎在这种抑制活性中很重要。

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