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CD80 expression and infiltrating regulatory T cells in idiopathic nephrotic syndrome of childhood

医学 局灶节段性肾小球硬化 免疫组织化学 肾病综合征 微小变化病 抗体 病理 活检 肾活检 抗原 发病机制 染色 肾小球硬化 肾小球肾炎 免疫学 内科学 蛋白尿
作者
Fehime Kara Eroğlu,Dıclehan Orhan,Mihriban İnözü,Ali Düzova,Bora Gülhan,Fatih Özaltın,Rezan Topaloğlu
出处
期刊:Pediatrics International [Wiley]
卷期号:61 (12): 1250-1256 被引量:15
标识
DOI:10.1111/ped.14005
摘要

Abstract Background CD 80 (also known as B7‐1) is a co‐stimulatory molecule that is expressed in biopsies and also excreted in urine in patients with minimal change disease ( MCD ) and focal segmental glomerulosclerosis ( FSGS ). CD 80 is inhibited by the cytotoxic T‐lymphocyte‐associated‐antigen 4 ( CTLA 4), which is mainly expressed on regulatory T cells (Tregs). Ineffective circulating Treg response is involved in the pathogenesis of nephrotic syndrome. In this study, we evaluated CD 80 expression and infiltrating Tregs in children with MCD and FSGS . Methods Evaluation of CD 80 expression and semi‐quantitative evaluation of Tregs ( FOXP 3‐positive CD 4 T cells) were carried out in 31 kidney biopsies (12 MCD , 19 FSGS ) with immunofluorescence and immunohistochemistry staining. Results All MCD sections were stained negative; whereas six out of 19 FSGS sections (all from steroid‐resistant ( SR ) patients), including one from a Wilms' tumor 1 ( WT 1) mutation‐positive FSGS patient, stained positive for anti‐ CD 80 goat antibody, and negative for anti‐ CD 80 rabbit antibody. FSGS biopsy specimens had significantly higher FOXP 3‐positive cells/mm 2 compared with MCD and control samples ( P < 0.001). Biopsy samples from SR ‐ FSGS patients ( n = 12) with positive CD 80 staining ( n = 6) had significantly less Tregs ( FOXP 3‐positive CD 4 T cells) compared with CD 80 (−) biopsies ( n = 6; P = 0.004). Conclusion CD 80 expression was not detected in the majority of the archival biopsy sections and the results were not consistent across the different antibodies. In the SR ‐ FSGS sections, however, CD 80‐positive biopsies had decreased FOXP 3‐positive CD 4 T cells, suggesting that a decreased anti‐inflammatory milieu may be the cause of increased CD 80 expression.
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