Laboratory of Microbiology and Molecular Genetics, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, Japan.
Department of Infectious Diseases, Medical Mycology Research Center, Chiba University, Chiba, Japan.
Front Immunol. 2020 Jan 21;10:3155. doi: 10.3389/fimmu.2019.03155. eCollection 2019.
In primary infection with , it has been reported-without consideration of 's functions-that humoral immunity plays no role in the clearance of bacteria. In fact, targets and suppresses several aspects of humoral immunity, including B cell lymphopoiesis, B cell activation, and IgG production. In particular, the suppression of IgG-secreting plasma cell maintenance allows the persistence of in tissues. Therefore, the critical role(s) of humoral immunity in the response to infection, especially at the late phase, should be re-investigated. The suppression of IgG plasma cell memory strongly hinders vaccine development against non-typhoidal (NTS) because can also reduce humoral immune memory against other bacteria and viruses, obtained from previous vaccination or infection. We propose a new vaccine against that would not impair humoral immunity, and which could also be used as a treatment for antibody-dependent autoimmune diseases to deplete pathogenic long-lived plasma cells, by utilizing the 's own suppression mechanism of humoral immunity.
在感染的初次阶段,据报道——并未考虑到的功能——体液免疫在清除细菌方面不起作用。事实上,靶向并抑制了体液免疫的几个方面,包括 B 细胞淋巴生成、B 细胞激活和 IgG 产生。特别是,抑制 IgG 分泌浆细胞的维持允许在组织中持续存在。因此,应该重新研究体液免疫在感染反应中的关键作用(特别是在后期阶段)。IgG 浆细胞记忆的抑制强烈阻碍了针对非伤寒沙门氏菌(NTS)的疫苗开发,因为也可以降低通过以前的疫苗接种或感染获得的针对其他细菌和病毒的体液免疫记忆。我们提出了一种针对的新型疫苗,该疫苗不会损害体液免疫,并且还可以作为治疗抗体依赖性自身免疫疾病的手段,通过利用自身抑制体液免疫的机制来耗尽致病性长寿浆细胞。