细胞免疫在Tamm－Horsfal蛋白所致肾小管间质性肾炎组织损伤中的作用

The Role of Cellular Immunity in the Tissue Damage ofTubulointerstitial Nephritis Caused by Tamm-Horsfall Protein

采用Ｔａｍｍ－Ｈｏｒｓｆａｌ蛋白（ＴＨＰ）直接肾内注射建立大鼠的小管间质性肾炎（ＴＩＮ）模型，ＴＩＮ组９只动物均发生小管间质性组织病理损伤，局灶性单核、淋巴细胞炎症细胞浸润；对照组仅１只轻度炎症改变。外周血Ｔ淋巴细胞免疫表型分析，术后７ｄＴＩＮ组与对照组间ＣＤ＋４、ＣＤ＋８、ＣＤ＋８－ＣＤ＋２５、ＣＤ＋８－Ｉａ＋抗原的表达及ＣＤ４／ＣＤ８的比值均无显著性差异（Ｐ＞０．０５），而术后１４ｄ、ＴＩＮ组均见升高，与对照组比差异有显著性（Ｐ＜０．０５），表明ＴＩＮ组出现Ｔ淋巴细胞的免疫应答反应和活化性细胞毒Ｔ细胞明显增加，从而证实ＴＨＰ在致ＴＩＮ免疫发病机制中，确实存在免疫系统激活。

Tubulointerstitial nephritis (TIN) was established in Wistar rats by direct intrarenal inoculation of TH protein. Focal TIN has heen found in all rats of the TIN group, the pathologic picture is focal infiltration of monocytes and lymphocytes, only one rat of the control group shows slight inflammatory change. Expression of T lymphocyte phenotype from the peripheral blood found there were no significant difference in the percentage of CD + 4,CD + 8,CD + 8-CD + 25 ,CD + 8-Ia the ratio of CD 4/CD 8 between the TIN group and the control group at the 7th day after intrarenal inoculation (P<0.05). But the expression of CD 4.CD 8/CD 25 ,CD 8-Ia and CD 4/CD 8 of the TIN group were higher than that of the control group at the 14th day,which indicate that the Tlymphocyte immune response has been happened. These results showed that the system of cellular immunity has been indeed activated in the pathogenetic mechanism of TIN induced by THP. It resulted in the damage of renal tissue.