Neisserial binding to CEACAM1 arrests the activation and proliferation of CD4+ T lymphocytes
Neisserial binding to CEACAM1 arrests the activation and proliferation of CD4+ T lymphocytes
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DOI：
10.1038/ni769
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发表时间：
2002-03-01
影响因子：
30.5
通讯作者：
Gray-Owen, SD
中科院分区：
文献类型：
--
作者：
Boulton, IC;Gray-Owen, SD
淋病奈瑟菌感染可引发强烈的炎症反应，但很少有特异性免疫反应或免疫记忆的发展。此外，淋病通常与血液中T淋巴细胞计数的短暂减少相关，当淋球菌感染消退时，这些人群会恢复。这些观察结果表明淋球菌对宿主免疫应答具有抑制作用。我们在这里报告说，N。淋球菌Opa蛋白能够结合由原代CD 4（+）T淋巴细胞表达的CEACAM 1并抑制其活化和增殖。CEACAM 1与淋球菌Opa结合（52），与酪氨酸磷酸酶SHP-1和SHP-2相关，这表明受体的ITIM（基于免疫受体酪氨酸的抑制基序）参与了这种作用。
Infection with Neisseria gonorrhoeae can trigger an intense inflammatory response, yet there is little specific immune response or development of immune memory. In addition, gonorrhea typically correlates with a transient reduction in T lymphocyte counts in blood, and these populations recover when gonococcal infection is resolved. Such observations suggest that the gonococci have a suppressive effect on the host immune response. We report here that N. gonorrhoeae O pa proteins were able to bind CEACAM1 expressed by primary CD4(+)T lymphocytes and suppress their activation and proliferation. CEACAM1 bound by gonococcal Opa(52) associated with the tyrosine phosphatases SHP-1 and SHP-2, which implicates the receptor's ITIM (immunoreceptor tyrosine-based inhibitory motif) in this effect.