Single-nucleotide polymorphisms of transforming growth factor-beta1 gene in Taiwanese patients with systemic lupus erythematosus.
Single-nucleotide polymorphisms of transforming growth factor-beta1 gene in Taiwanese patients with systemic lupus erythematosus.
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台湾系统性红斑狼疮患者转化生长因子-β1 基因的单核苷酸多态性。
DOI：
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Angela Chen
中科院分区：
文献类型：
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作者：
Ling;He‐Hsiung Cheng;P. Sung;Jeng;Y. Shiue;Angela Chen
转化生长因子-β1(TGF-β1)参与了CD8+T抑制细胞、自然杀伤(NK)细胞和调节性T(Th3)细胞的产生，从而下调抗体的产生。我们研究了系统性红斑狼疮(SLE)患者体内转化生长因子-β1的活性，试图阐明转化生长因子-β1的调节失调是否由遗传因素决定。对55例服用微量类固醇和/或羟氯喹的临床缓解期SLE患者和40例健康对照的血清，以及18例SLE患者和10例正常对照的刀豆蛋白A刺激的外周血单核细胞培养上清液进行了转化生长因子-β1的酶联免疫吸附试验。对138例SLE患者和182例对照组的转化生长因子-β1基因-988C/A、-800G/A、-509C/T、Leu10/Pro10和Arg25/Pro25 5个单核苷酸多态(SNPs)进行了基因分型。系统性红斑狼疮患者血清转化生长因子-β1水平低于正常对照组(P=0.052)。SLE患者PBMC未刺激和刺激后产生的转化生长因子-β1均高于对照组，但差异无统计学意义(P分别为0.073和0.074)。在台湾患者中，没有一种转化生长因子-β1单核苷酸多态与系统性红斑狼疮密切相关，也没有对狼疮性肾炎的预后有任何意义。因此，这些多态并不代表SLE的遗传易感性。在台湾临床稳定的SLE患者中，推测通过产生PBMC转化生长因子-β1来调节自发性B细胞过度活动的固有能力是完整的。导致SLE免疫调节缺陷的较低血清转化生长因子-β1水平是否主要受遗传控制，或次要于细胞因子环境中正在进行的细胞相互作用的影响，尚需阐明。
Transforming growth factor-beta1 (TGF-beta1) is involved in the generation of CD8+ T suppressor cells, natural killer (NK) cells and regulatory T (Th3) cells for down-regulatory effects on antibody production. We studied TGF-beta1 activity in patients with systemic lupus erythematosus (SLE) to try to clarify whether the dysregulation by TGF-beta1 is genetically determined. Sera from 55 patients with clinically inactive SLE, who were taking minimal steroids and/or hydroxychloroquine, and 40 healthy controls, along with supernatants from concanavalin A-stimulated peripheral blood mononuclear cell (PBMC) cultures from 18 patients with SLE and 10 controls were subjected to TGF-beta1 enzyme-linked immunosorbent assay. A total of 138 patients with SLE and 182 controls were genotyped for 5 single-nucleotide polymorphisms (SNPs) of TGF-beta1: -988C/A, -800G/A, -509C/T, Leu10/Pro10 and Arg25/Pro25. Patients with SLE had lower serum levels of TGF-beta1 compared with controls (p=0.052). The unstimulated and stimulated TGF-beta1 production of PBMCs in patients with SLE was higher than in controls, although these differences did not reach significance (p=0.073 and 0.074, respectively). None of the TGF-beta1 SNPs was strongly associated with SLE in Taiwanese patients or had any prognostic significance in lupus nephritis. Hence these polymorphisms do not represent a genetic predisposition to SLE. The intrinsic capability of immunoregulation for spontaneous B cell hyperactivity through PBMC TGF-beta1 production was presumed to be intact in clinically stable SLE in Taiwanese. Whether the lower serum TGF-beta1 level that causes the defective immune regulation in SLE is primarily under genetic control or secondary to the influence of ongoing cellular interactions in the cytokine context needs to be elucidated.
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影响因子：
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作者：
Sleasman,JW;Henderson,M;Barrett,DJ
通讯作者：
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影响因子：
4.4
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DOI：
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发表时间：
1995
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
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作者：
Nunes,I;Shapiro,RL;Rifkin,DB
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DOI：
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发表时间：
1993
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Lee,HM;Rich,S
通讯作者：
Rich,S