布氏锥虫感染耗竭记忆B细胞导致宿主无法回忆保护性B细胞反应。

S. Moon, I. Janssens, K. Kim, B. Stijlemans, S. Magez, M. Radwanska
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引用次数: 5

摘要

背景:布氏锥虫(T. B . brucei)通过多种方式逃避宿主免疫反应,包括破坏B细胞稳态。这阻碍了抗锥虫疫苗的开发。由于这种病理背后的细胞机制从未被解决,我们的研究集中在接种过锥虫的小鼠的记忆B细胞(MBCs)的命运。方法采用sa锥虫变异表面糖蛋白(VSG)和荧光藻红蛋白(PE)作为免疫抗原。研究了同种和异种寄生虫侵染后抗原特异性MBCs的功能和细胞特性。结果AnTat 1.1 VSG可触发特异性抗体反应和CD73 +CD273 +CD80 + MBCs的同型转换,对同源寄生虫的攻击提供90%的无菌保护。正如预期的那样,AnTat 1.1 VSG免疫不能预防异源VSG转换寄生虫的感染。在成功的治愈性药物治疗后,小鼠显示完全失去了先前诱导的对同源寄生虫的保护性免疫,与疫苗诱导的MBCs的丧失相一致。PE免疫方法证实,锥虫感染导致抗原特异性的脾和骨髓MBCs的普遍损失,以及抗原特异性igg的减少。结论锥虫病可引起全身性免疫记忆丧失。这有利于寄生虫减少对抗原变异要求的严格程度。
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Trypanosoma brucei brucei Infection Depletes Memory B Cells Resulting in Inability of the Host to Recall Protective B Cells Responses.
BACKGROUND Trypanosoma brucei brucei (T. b. brucei) evades host immune responses by multiple means, including the disruption of B cell homeostasis. This hampers anti-trypanosome vaccine development. As the cellular mechanism underlying this pathology has never been addressed, our study focuses on the fate of memory B cells (MBCs) in vaccinated mice upon trypanosome challenge. METHODS A trypanosome variant surface glycoprotein (VSG) and fluorescent phycoerythrin (PE) were used as immunization antigens. Functional and cellular characteristics of antigen-specific MBCs were studied after homologous and heterologous parasite challenge. RESULTS Immunization with AnTat 1.1 VSG triggers a specific antibody response and isotype-switched CD73 +CD273 +CD80 + MBCs, delivering 90% sterile protection against a homologous parasite challenge. As expected, AnTat 1.1 VSG immunization does not protect against infection with heterologous VSG-switched parasites. After successful curative drug treatment, mice were shown to have completely lost their previously induced protective immunity against the homologous parasites, coinciding with the loss of vaccine-induced MBCs. A PE immunization approach confirmed that trypanosome infections cause the general loss of antigen-specific splenic and bone marrow MBCs, and a reduction in antigen-specific IgGs. CONCLUSION Trypanosomosis induces general immunological memory loss. This benefits the parasites by reducing the stringency for antigenic variation requirements.
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