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终末期肾病患者中甲状旁腺激素(PTH)对T细胞活化的影响

T-cell activation modified by parathyroid hormone (PTH) in patients with end-stage renal disease.

作者信息

Kaneko T, Osono E, Hayama N, Lino Y, Terashi A

机构信息

Second Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.

出版信息

Clin Nephrol. 1997 Dec;48(6):353-8.

PMID:9438093
Abstract

We studied the effect of parathyroid hormone (PTH) on the proliferation of T cells from patients with end-stage renal disease (ESRD) (n = 16) and normal subjects (n = 20). In patients with ESRD, T-cell proliferation expressed as stimulation index (SI) was significantly decreased from 99.2 +/- 31.2 to 46.3 +/- 10.8, when 10 ng/ml of recombinant PTH (rPTH) was added in vitro. The reduction of SI with rPTH was dose dependent. However, in normal subjects, the SI was increased from 56.2 +/- 13.6 to 67.9 +/- 16.5 (p < 0.01) by addition of rPTH. These findings were also shown by allo or specific antigen-induced T-cell stimulation. When T cells from normal subjects were pretreated with 10 ng/ml of PTH, with 100 mg/dl of urea or with a condition of pH 7.0, the effect of rPTH was changed to decrease the T-cell proliferation induced by anti-CD3 antibody. These data suggested that uremic state, including hyperparathyroidism, changed the response of T cells against PTH.

摘要

我们研究了甲状旁腺激素(PTH)对终末期肾病(ESRD)患者(n = 16)和正常受试者(n = 20)T细胞增殖的影响。在ESRD患者中,当体外添加10 ng/ml重组PTH(rPTH)时,以刺激指数(SI)表示的T细胞增殖从99.2±31.2显著降低至46.3±10.8。rPTH导致的SI降低呈剂量依赖性。然而,在正常受试者中,添加rPTH后SI从56.2±13.6增加至67.9±16.5(p < 0.01)。这些结果在同种异体或特异性抗原诱导的T细胞刺激中也得到了证实。当正常受试者的T细胞用10 ng/ml PTH、100 mg/dl尿素预处理或处于pH 7.0条件下时,rPTH的作用转变为降低抗CD3抗体诱导的T细胞增殖。这些数据表明,包括甲状旁腺功能亢进在内的尿毒症状态改变了T细胞对PTH的反应。

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