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协同刺激因子B7在药物性间质性肾炎和IgA肾病间质损伤中的作用 被引量:3

Costimulatory B7 molecules in drug induced interstitial nephritis and IgA nephropathy with tubulointerstitial injury
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摘要 目的探讨协同刺激因子B7介导的免疫反应在药物性间质性肾炎和IgA肾病间质损伤发生中的作用。方法应用免疫组织化学方法对药物性间质性肾炎,IgA肾病伴肾小管间质损伤(IgAN)患者和正常人肾组织中协同刺激因子B7-1和B7-2,HLA-DR抗原以及CD4+和CD8+细胞的分布进行了观察和分析。结果间质性肾炎患者肾间质CD4+和CD8+细胞浸润明显增加,表达B7-1和B7-2的细胞显著增多,同时伴肾小管上皮细胞HLA-DR和B7-1表达的增加。IgAN患者肾间质中CD4+和CD8+细胞较正常人增多,表达B7-1的细胞无明显差异。肾小管上B7-1的表达有所增加,但HLA-DR的表达不增加。结论药物性间质性肾炎和IgAN患者肾小管及间质免疫损伤的表现形式及发生机理存在着差异。 Objective To evaluate the role of costimulatory B7 molecules in the pathogenesis of drug induced interstitial nephritis(D TIN) and IgA nephropathy with severe tubulointerstitial injury(IgAN).Methods Renal biopsy materials from D TIN(n=15) and IgAN(n=15) were used. Cadaveric donors for kidney transplantation(n=10) served as normal controls.The lymphocyte subsets and the expression of B7 1, B7 2 and HLA DR in the renal tissue were analyzed by immunohistochemistry staining. Results CD4 + and CD8 + cells in the interstitium markedly increased in patients with D TIN. Parallelly,B7 1 and B7 2 expressing cells in the interstitium also augmented in this group of patients.The expression of B7 1 and HLA DR on the renal tubular cells increased in patients with D TIN. Although CD4 + and CD8 + cells increased in the interstitium of IgAN,the B7 1 and B7 2 expressing cells in the interstitium were not different from those of the normal controls. Although the renal tubular expression of B7 1 was upregulated in IgAN,the expression of HLA DR kept in the normal range. Conclusion These results indicate that the costimulatory molecules mediated T cell activation plays an important role in the pathogenesis of D TIN. The interstitial infiltrating and tubular cells both act as an antigen presenting cells in the initiation of immune injury in D TIN. However, such evidence has not been found in patients with IgAN.
出处 《中华医学杂志》 CAS CSCD 北大核心 1998年第7期517-519,共3页 National Medical Journal of China
基金 全军"九五"重点课题资助
关键词 肾小球肾炎 间质性肾炎 协同刺激因子B7 Nephritis, interstitial Glomerulonephritis IgA
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参考文献2

  • 1Deng A,J Am Sci Nephrol,1996年,7期,1696页
  • 2Huang A Y,J Exp Med,1996年,183卷,769页

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