...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Neisseria gonorrhoeae Kills Carcinoembryonic Antigen-Related Cellular Adhesion Molecule 1 (CD66a)-Expressing Human B Cells and Inhibits Antibody Production
【24h】

Neisseria gonorrhoeae Kills Carcinoembryonic Antigen-Related Cellular Adhesion Molecule 1 (CD66a)-Expressing Human B Cells and Inhibits Antibody Production

机译：淋病奈瑟氏菌杀死表达癌胚抗原相关细胞粘附分子1（CD66a）的人B细胞并抑制抗体产生。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Neisseria gonorrhoeae cells (gonococci [GC]), the etiological agents for gonorrhea, can cause repeated infections. During and after gonococcal infection, local and systemic antigonococcal antibody levels are low. These clinical data indicate the possibility that GC may suppress immune responses during infection. Carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1 or CD66a), a receptor for GC opacity (Opa) proteins, was shown to mediate inhibitory signals. In the present study, human B cells were activated by interleukin-2 to express CEACAM1 and then stimulated to secrete antibodies and simultaneously coincubated with Opa? and OpaI GC of strain MS11. Our results show that this OpaI GC has the ability to inhibit antibody production. The interaction of GC and CEACAM1 with human peripheral B cells also results in induction of cell death. The same findings were observed in DT40 B cells. This CEACAM1-promoted cell death pathway does not involve the inhibitory signals or the tyrosine phosphatases SHP-1 and SHP-2 but depends on Bruton's tyrosine kinase in DT40 cells. Our results suggest that Neisseria gonorrhoeae possesses the ability to suppress antibody production by killing CEACAM1-expressing B cells.
机译：淋病的病原体淋病奈瑟氏球菌（gonococci [GC]）可引起反复感染。淋球菌感染期间和之后，局部和全身性抗淋球菌抗体水平较低。这些临床数据表明，GC可能会抑制感染期间的免疫反应。癌胚抗原相关的细胞粘附分子1（CEACAM1或CD66a）是GC不透明（Opa）蛋白的受体，被证明可以介导抑制信号。在本研究中，人白细胞被白介素2激活以表达CEACAM1，然后被刺激分泌抗体，同时与MS11菌株的Opa ？和OpaI GC共孵育。我们的结果表明，该OpaI GC具有抑制抗体产生的能力。 GC和CEACAM1与人外周血B细胞的相互作用也导致细胞死亡的诱导。在DT40 B细胞中观察到相同的发现。此CEACAM1促进的细胞死亡途径不涉及抑制信号或酪氨酸磷酸酶SHP-1和SHP-2，但取决于DT40细胞中的Bruton酪氨酸激酶。我们的结果表明，淋病奈瑟氏球菌具有通过杀死表达CEACAM1的B细胞来抑制抗体产生的能力。

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