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IgA肾病患者T淋巴细胞中白细胞介素-2受体表达的体外研究。

In vitro study of expression of interleukin-2 receptors in T-lymphocytes from patients with IgA nephropathy.

作者信息

Lai K N, Leung J C, Lai F M

机构信息

Department of Medicine, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin.

出版信息

Clin Nephrol. 1988 Dec;30(6):330-4.

PMID:2977310
Abstract

The present study was undertaken to examine the expression of interleukin-2 receptor (IL-2R)/CD25 antigen in cultured T-lymphocyte subsets in IgA nephropathy. Twenty-four IgA nephritic patients, 12 patients with chronic glomerulonephritis (non-IgA nephropathy), and 17 healthy controls were studied in an infection-free interval. T-cell subsets in peripheral blood mononuclear cells (PBMC) and activated T-lymphocyte subsets expressing IL-2R were determined by double immunofluorescence staining with fluorochromes conjugated to monoclonal antibodies against T-helper/inducer (CD4+) cell, T-suppressor/cytotoxic (CD8+) cell, B (CD20+) lymphocytes, and IL-2R. The percentages of CD4+ and CD8+ lymphocytes, CD4/CD8 ratio, and total activated lymphocytes (with IL-2R/CD25 antigen) did not differ between the IgA nephritic patients, patients with chronic glomerulonephritis, and healthy controls in freshly isolated, unstimulated lymphocytes or PBMC cultured with pokeweed mitogen. Following pokeweed mitogen stimulation for 5 days, 17.3 +/- 10.3%, 16.6 +/- 8.4%, and 16.7 +/- 9.4% of PBMC from IgA nephritic patients, patients with chronic glomerulonephritis, and controls respectively expressed IL-2R (p greater than 0.05). However, the individual T-cell subsets bearing IL-2R were distinctly different between the IgA nephritic patients and patients with chronic glomerulonephritis or healthy controls. IgA nephritic patients had increased activated CD4+ lymphocytes (with IL-2R) (p less than 0.025) and reduced activated CD8+ lymphocytes (p less than 0.025). Our study suggests a defective immunoregulation in IgA nephropathy with enhanced T-helper/inducer and reduced T-suppressor/cytotoxic activity when stimulated with mitogen and probably, during clinical exacerbation.

摘要

本研究旨在检测白细胞介素-2受体(IL-2R)/CD25抗原在IgA肾病培养的T淋巴细胞亚群中的表达。在无感染间期,对24例IgA肾病患者、12例慢性肾小球肾炎(非IgA肾病)患者和17名健康对照者进行了研究。通过用与抗T辅助/诱导(CD4+)细胞、T抑制/细胞毒性(CD8+)细胞、B(CD20+)淋巴细胞和IL-2R的单克隆抗体偶联的荧光染料进行双重免疫荧光染色,测定外周血单个核细胞(PBMC)中的T细胞亚群和表达IL-2R的活化T淋巴细胞亚群。在新鲜分离的、未刺激的淋巴细胞或用商陆有丝分裂原培养的PBMC中,IgA肾病患者、慢性肾小球肾炎患者和健康对照者的CD4+和CD8+淋巴细胞百分比、CD4/CD8比值以及总活化淋巴细胞(带有IL-2R/CD25抗原)并无差异。在用商陆有丝分裂原刺激5天后,IgA肾病患者、慢性肾小球肾炎患者和对照者的PBMC分别有17.3±10.3%、16.6±8.4%和16.7±9.4%表达IL-2R(p>0.05)。然而,IgA肾病患者与慢性肾小球肾炎患者或健康对照者之间,带有IL-2R的单个T细胞亚群明显不同。IgA肾病患者活化的CD4+淋巴细胞(带有IL-2R)增加(p<0.025),而活化的CD8+淋巴细胞减少(p<0.025)。我们的研究提示,IgA肾病存在免疫调节缺陷,在用有丝分裂原刺激时,可能在临床病情加重期间,T辅助/诱导活性增强,T抑制/细胞毒性活性降低。

相似文献

1
In vitro study of expression of interleukin-2 receptors in T-lymphocytes from patients with IgA nephropathy.IgA肾病患者T淋巴细胞中白细胞介素-2受体表达的体外研究。
Clin Nephrol. 1988 Dec;30(6):330-4.
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引用本文的文献

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Increase of both circulating Th1 and Th2 T lymphocyte subsets in IgA nephropathy.IgA肾病中循环Th1和Th2 T淋巴细胞亚群均增加。
Clin Exp Immunol. 1994 Apr;96(1):116-21. doi: 10.1111/j.1365-2249.1994.tb06240.x.
2
T-cell subsets, interleukin-2 receptor expression and production of interleukin-2 in minimal change nephrotic syndrome.微小病变型肾病中的T细胞亚群、白细胞介素-2受体表达及白细胞介素-2产生
Pediatr Nephrol. 1994 Dec;8(6):649-52. doi: 10.1007/BF00869075.
3
T-lymphocyte activation in IgA nephropathy: serum-soluble interleukin 2 receptor level, interleukin 2 production, and interleukin 2 receptor expression by cultured lymphocytes.
IgA肾病中的T淋巴细胞激活:血清可溶性白细胞介素2受体水平、白细胞介素2产生及培养淋巴细胞的白细胞介素2受体表达
J Clin Immunol. 1989 Nov;9(6):485-92. doi: 10.1007/BF00918018.
4
Light-chain ratio of serum IgA1 in IgA nephropathy.IgA肾病中血清IgA1的轻链比例
J Clin Immunol. 1991 Jul;11(4):219-23. doi: 10.1007/BF00917428.
5
Cytokine production by peripheral blood mononuclear cells in IgA nephropathy.IgA肾病中外周血单个核细胞的细胞因子产生
Clin Exp Immunol. 1991 Aug;85(2):240-5. doi: 10.1111/j.1365-2249.1991.tb05712.x.
6
Production of interleukin-2 (IL-2) and expression of IL-2 receptor in patients with IgA nephropathy.IgA肾病患者白细胞介素-2(IL-2)的产生及IL-2受体的表达
Korean J Intern Med. 1992 Jan;7(1):31-8. doi: 10.3904/kjim.1992.7.1.31.