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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Thymic microenvironment and NZB mice: the abnormal thymic microenvironment of New Zealand mice correlates with immunopathology.
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Thymic microenvironment and NZB mice: the abnormal thymic microenvironment of New Zealand mice correlates with immunopathology.

机译：胸腺微环境和NZB小鼠：新西兰小鼠的胸腺微环境异常与免疫病理学相关。

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There are distinct microenvironmental abnormalities of thymic architecture in several murine models of SLE defined using immunohistochemistry and a panel of mAb dissected at thymic epithelial markers. To address the issue of the relationship between the thymic microenvironment and autoimmunity, we studied backcross (NZB x NZW) F1 x NZW mice in which 50% of offspring develop nephritis associated with proteinuria and anti-DNA antibodies. We reasoned that if thymic abnormalities are associated with development of disease, the correlation of abnormalities with lupus-like disease in individual backcross mice will form the foundation for identification of the mechanisms involved. In parallel, we directed a genetic linkage analysis, using markers previously shown to be linked to nephritis and IgG autoantibody production, to determine if such loci were similarly associated with microenvironmental changes. Our data demonstrate that all (NZB x NZW) F1 x NZW backcross mice with disease have microenvironmental defects. Although the microenvironmental defects are not sufficient for development of autoimmune disease, the severity of thymic abnormalities correlates with titers of IgG autoantibodies to DNA and with proteinuria. Consistent with past studies of (NZB x NZW) F1 x NZW mice, genetic markers on proximal chromosome 17 (near MHC) and distal chromosome 4 showed trends for linkage with nephritis. Although the markers chosen only covered about 10-15% of the genome, the results demonstrated trends for linkage with thymic medullary abnormalities for loci on distal chromosome 4 and distal chromosome 1. We believe it will be important to define the biochemical nature of the molecules recognized by these mAbs to understand the relationships between thymic architecture and immunopathology. Copyright 1999 Academic Press.
机译：在使用免疫组织化学和在胸腺上皮标记物上解剖的一组mAb定义的几种SLE鼠模型中，胸腺结构的微环境异常异常。为了解决胸腺微环境与自身免疫之间关系的问题，我们研究了回交（NZB x NZW）F1 x NZW小鼠，其中50％的后代发展为蛋白尿和抗DNA抗体相关的肾炎。我们认为，如果胸腺异常与疾病的发展有关，则个体回交小鼠中异常与狼疮样疾病的相关性将为鉴定所涉及的机制奠定基础。同时，我们进行了遗传连锁分析，使用先前显示与肾炎和IgG自身抗体产生相关的标记，确定这种基因座是否与微环境变化相似。我们的数据表明，所有（NZB x NZW）F1 x NZW回交小鼠均患有微环境缺陷。尽管微环境缺陷不足以发展自身免疫性疾病，但胸腺异常的严重程度与针对DNA的IgG自身抗体的滴度和蛋白尿有关。与过去对（NZB x NZW）F1 x NZW小鼠的研究一致，近端17号染色​​体（靠近MHC）和4号染色体上的遗传标记显示出与肾炎连锁的趋势。尽管选择的标记仅覆盖基因组的约10-15％，但结果表明与远端4号染色体和1号远端染色体上的胸腺髓样异常联系的趋势。我们认为定义分子的生化性质将很重要被这些mAb识别以了解胸腺结构与免疫病理之间的关系。版权所有1999，学术出版社。

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