...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of investigative dermatology. >Identification of quantitative trait loci in experimental epidermolysis bullosa acquisita
【24h】

Identification of quantitative trait loci in experimental epidermolysis bullosa acquisita

机译：实验性表皮松解大疱中数量性状基因座的鉴定

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Epidermolysis bullosa acquisita (EBA) is a chronic mucocutaneous autoimmune skin blistering disease. Several lines of evidence underscore the contribution of autoantibodies against type VII collagen (COL7) to the pathogenesis of EBA. Furthermore, EBA susceptibility is associated with the MHC haplotype in patients (HLA-DR2) and in immunization-induced EBA in mice (H2s). The latter study indicated an additional contribution of non-MHC genes to disease susceptibility. To identify non-MHC genes controlling EBA susceptibility, we intercrossed EBA-susceptible MRL/MpJ with EBA-resistant NZM2410/J and BXD2/TyJ as well as Cast mice. Mice of the fourth generation of this four-way autoimmune-prone advanced intercross line were immunized with a fragment of murine COL7 to induce EBA. Anti-COL7 autoantibodies were detected in 84% of mice, whereas deposition of complement at the dermal-epidermal junction (DEJ) was observed in 50% of the animals; 33% of immunized mice presented with overt clinical EBA. Onset of clinical disease was associated with several quantitative trait loci (QTLs) located on chromosomes 9, 12, 14, and 19, whereas maximum disease severity was linked to QTLs on chromosomes 1, 15, and 19. This more detailed insight into the pathogenesis of EBA may eventually lead to new treatment strategies for EBA and other autoantibody-mediated diseases.
机译：大疱表皮松解症（EBA）是一种慢性粘膜皮肤自身免疫性皮肤水疱病。几项证据强调了针对VII型胶原（COL7）的自身抗体对EBA发​​病的贡献。此外，EBA易感性与患者的MHC单倍型（HLA-DR2）和小鼠的免疫诱导EBA（H2s）有关。后一项研究表明非MHC基因对疾病易感性的额外贡献。为了鉴定控制EBA敏感性的非MHC基因，我们将EBA敏感性MRL / MpJ与抗EBA的NZM2410 / J和BXD2 / TyJ以及Cast小鼠杂交。用鼠COL7的片段免疫该易产生四向自身免疫的高级交叉杂交系的第四代小鼠，以诱导EBA。在84％的小鼠中检测到了抗COL7自身抗体，而在50％的动物中观察到了补体在真皮-表皮连接处（DEJ）的沉积。 33％的免疫小鼠表现出明显的临床EBA。临床疾病的发作与位于染色体9、12、14和19上的几个定量性状位点（QTL）相关，而最大的疾病严重程度与染色体1、15和19上的QTL相关。 EBA的出现可能最终导致针对EBA和其他自身抗体介导的疾病的新治疗策略。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号