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我们在体外试验中证实：Ｔａｍｍ－Ｈｏｒｓｆａｌｌ蛋白（ＴＨＰ）刺激人单核细胞产生肿瘤坏死因子和ＩＬ－１的作用依赖其糖基组分的完整。为了探讨糖基组分在ＴＨｐ所致肾小管间质肾炎（ＴＩＮ）发病机制中的作用。我们给Ｗｉｓｔａｒ大鼠肾内直接注射ＴＨＰ制成ＴＩＮ模型。该模型在发病第４ｄ即有明显的肾间质巨噬细胞（ＭΦ）浸润。用高碘酸氢化去除ＴＨＰ的糖基组分明显破坏了ＴＨＰ诱发ＴＩＮ的能力。注射去糖基ＴＨＰ的动物只有轻微的组织学和超微结构改变。肾间质浸润的ＭΦ数量明显减少，亦无肾小管功能障碍。由此表明：ＴＨＰ的糖基组分在其导致ＴＩＮ的发生、发展中具有关键作用。
We demonstrate in vitro that the effect of Tamm-Horsfall protein (THP) on the production of tumor necrosis factor and IL-1 by human monocytes depends on the integrity of their glycosylation components. To explore the role of glycosyl moiety in the pathogenesis of THp-induced tubulointerstitial nephritis (TIN). We injected Wistar rats directly with THP into the model of TIN. The model in the onset of 4d obvious interstitial macrophage (MΦ) infiltration. Hydrogenation of periodate to remove the glycosyl component of THP significantly disrupts the ability of THP to induce TIN. Animals injected with the deglycosylated THP had only slight histological and ultrastructural changes. MΦ interstitial infiltration significantly reduced the number, nor renal tubular dysfunction. This shows that: THP glycosyl component in the TIN led to its occurrence, the development of a key role.