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通过早期DNA免疫和注射细菌脂多糖加速NZB×NZW小鼠的肾小球肾炎。利用NZB×NZW小鼠疾病的加速模型治疗狼疮性肾炎的实验方法。

Acceleration of glomerulonephritis in NZB x NZW mice by early immunization with DNA and injection of bacterial lipopolysaccharide. Experimental approach to the treatment of lupus nephritis by use of the accelerated model of NZB x NZW mouse disease.

作者信息

Fournie G J, Minh M G, Mignon-Conte M A, Hass S, Lambert P H, Conte J J

出版信息

J Clin Lab Immunol. 1980 Sep;4(2):103-6.

PMID:7441709
Abstract

The effects of early immunization with DNA and of injection of bacterial lipopolysaccharide (LPS) on the glomerulonephritis of NZB x NZW mice were studied. Combined injections of DNA complexed to methylated bovine serum albumin (DNA-mBSA) and of LPS appeared to be more efficient in accelerating the disease in NZB x NZW mice than injections of DNA-mBSA or LPS alone. A rapid increase in levels of anti-DNA antibodies, an early appearance of severe renal lesions and a shortened survival were observed in mice injected with both DNA-mBSA and LPS. This new model was found to be suitable for therapeutic studies in mice with accelerated disease treated with cyclophosphamide and heparin. The efficacy of cyclophosphamide for the treatment of NZB x NZW mouse disease was shown by immunological and histological studies in mice younger than 4 months. Heparin appeared to have a beneficial effect by preventing the endocapillary cellular proliferation induced by injections of DNA-mBSA and LPS. The accelerated model of NZB x NZW mouse disease might be a useful tool for experiments on the treatment of lupus nephritis.

摘要

研究了DNA早期免疫及注射细菌脂多糖(LPS)对NZB×NZW小鼠肾小球肾炎的影响。与甲基化牛血清白蛋白复合的DNA(DNA-mBSA)和LPS联合注射,在加速NZB×NZW小鼠疾病进展方面似乎比单独注射DNA-mBSA或LPS更有效。在同时注射DNA-mBSA和LPS的小鼠中,观察到抗DNA抗体水平迅速升高、严重肾损伤早期出现以及生存期缩短。发现这种新模型适用于用环磷酰胺和肝素治疗的疾病加速小鼠的治疗研究。4个月以下小鼠的免疫学和组织学研究表明了环磷酰胺治疗NZB×NZW小鼠疾病的疗效。肝素似乎具有有益作用,可防止因注射DNA-mBSA和LPS诱导的毛细血管内细胞增殖。NZB×NZW小鼠疾病的加速模型可能是狼疮性肾炎治疗实验的有用工具。

相似文献

1
Acceleration of glomerulonephritis in NZB x NZW mice by early immunization with DNA and injection of bacterial lipopolysaccharide. Experimental approach to the treatment of lupus nephritis by use of the accelerated model of NZB x NZW mouse disease.通过早期DNA免疫和注射细菌脂多糖加速NZB×NZW小鼠的肾小球肾炎。利用NZB×NZW小鼠疾病的加速模型治疗狼疮性肾炎的实验方法。
J Clin Lab Immunol. 1980 Sep;4(2):103-6.
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Reduced fragmentation of apoptotic chromatin is associated with nephritis in lupus-prone (NZB x NZW)F(1) mice.凋亡染色质片段化减少与狼疮易感(NZB×NZW)F1小鼠的肾炎有关。
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CXCR3 promotes the production of IgG1 autoantibodies but is not essential for the development of lupus nephritis in NZB/NZW mice.CXCR3促进IgG1自身抗体的产生,但对NZB/NZW小鼠狼疮性肾炎的发展并非必不可少。
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Reversal of ongoing proteinuria in autoimmune mice by treatment with C-reactive protein.通过用C反应蛋白治疗使自身免疫小鼠正在进行的蛋白尿逆转。
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Treatment of lupus nephritis in adult (NZB + NZW)F1 mice by cortisone-facilitated tolerance to nucleic acid antigens.通过可的松促进对核酸抗原的耐受性来治疗成年(NZB + NZW)F1小鼠的狼疮性肾炎。
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Genetic studies of autoimmunity in New Zealand mice. III. Associations among anti-DNA antibodies, NTA, and renal disease in (NZB x NZW)F1 x NZW backcross mice.新西兰小鼠自身免疫的遗传学研究。III. (NZB×NZW)F1×NZW回交小鼠中抗DNA抗体、NTA与肾脏疾病之间的关联
J Immunol. 1981 Aug;127(2):433-7.

引用本文的文献

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2
Lipidome modulation by dietary omega-3 polyunsaturated fatty acid supplementation or selective soluble epoxide hydrolase inhibition suppresses rough LPS-accelerated glomerulonephritis in lupus-prone mice.膳食ω-3 多不饱和脂肪酸补充或选择性可溶性环氧化物水解酶抑制调节脂类组抑制狼疮易感小鼠粗糙 LPS 加速性肾小球肾炎。
Front Immunol. 2023 Feb 16;14:1124910. doi: 10.3389/fimmu.2023.1124910. eCollection 2023.
3
Mesangial cells of lupus-prone mice are sensitive to chemokine production.
狼疮易感小鼠的系膜细胞对趋化因子的产生敏感。
Arthritis Res Ther. 2007;9(4):R67. doi: 10.1186/ar2226.
4
Modulation of renal disease in autoimmune NZB/NZW mice by immunization with bacterial DNA.通过用细菌DNA免疫对自身免疫性NZB/NZW小鼠的肾脏疾病进行调节。
J Exp Med. 1996 Apr 1;183(4):1389-97. doi: 10.1084/jem.183.4.1389.
5
Accelerated (proliferative) lupus nephritis.加速性(增殖性)狼疮性肾炎。
Am J Pathol. 1990 Dec;137(6):1549-51.
6
Bacterial lipopolysaccharide induces long-lasting IgA deficiency concurrently with features of polyclonal B cell activation in normal and in lupus-prone mice.细菌脂多糖在正常小鼠和易患狼疮的小鼠中,诱导持久的IgA缺乏,同时伴有多克隆B细胞激活的特征。
Clin Exp Immunol. 1991 Apr;84(1):134-8.