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肾小球肾炎患者单核细胞释放肿瘤坏死因子-α增加。

Increased release of tumor necrosis factor-alpha by monocytes from patients with glomerulonephritis.

作者信息

Matsumoto K

机构信息

Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.

出版信息

Clin Nephrol. 1993 Sep;40(3):148-54.

PMID:8403569
Abstract

The release of tumor necrosis factor-alpha (TNF) was measured in supernatants of cultured peripheral blood monocytes (PBM) that were obtained from patients with glomerulonephritis (GN) and healthy controls. Spontaneous and lipopolysaccharide (LPS)-induced TNF release were significantly higher in PBM isolated from patients with IgA nephropathy (IgA N) and membranous nephropathy (MN) as compared to normal controls. These biological activities were neutralized by a specific antibody to TNF. In patients with IgA N and MN TNF levels did not correlate with clinical disease activity. We conclude that in vitro GN PBM are hyperactive in their release of TNF, and that this enhanced release of TNF in vitro may reflect a secondary consequence of monocyte activation rather than a primary cellular defect in GN.

摘要

在从肾小球肾炎(GN)患者和健康对照者获取的培养外周血单核细胞(PBM)的上清液中,检测肿瘤坏死因子-α(TNF)的释放情况。与正常对照相比,从IgA肾病(IgA N)和膜性肾病(MN)患者分离出的PBM中,自发性和脂多糖(LPS)诱导的TNF释放显著更高。这些生物活性被TNF特异性抗体中和。在IgA N和MN患者中,TNF水平与临床疾病活动度无关。我们得出结论,体外GN的PBM在TNF释放方面功能亢进,并且体外TNF释放增强可能反映单核细胞活化的继发性后果,而非GN中的原发性细胞缺陷。

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