United States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.
PLoS One. 2020 Sep 4;15(9):e0238493. doi: 10.1371/journal.pone.0238493. eCollection 2020.
To better understand anti-malaria protective immune responses, we examined the cellular mechanisms that govern protective immunity in a murine Plasmodium yoelii 17X NL (PyNL) re-infection model. Initially, we confirmed that immune B cells generated during a primary PyNL infection were largely responsible for protection from a second PyNL infection. Using the previously identified memory B cell markers CD80, PD-L2, and CD73, we found an increase in the frequency of CD80-PD-L2-CD73+ B cells up to 55 days after a primary PyNL infection and at 4-6 days following a second PyNL infection. Moreover, injection of enriched immune CD19+CD73+ B cells into nonimmune mice were significantly more protective against a PyNL infection than CD73- B cells. Interestingly, a substantial fraction of these CD73+ B cells also expressed IgM and granzyme B, a biomolecule that has been increasingly associated with protective responses against malaria.
为了更好地理解抗疟保护免疫反应，我们研究了控制小鼠疟原虫 yoelii 17X NL（PyNL）再感染模型中保护性免疫的细胞机制。最初，我们证实，在原发性 PyNL 感染期间产生的免疫 B 细胞在很大程度上负责免受第二次 PyNL 感染。使用先前鉴定的记忆 B 细胞标志物 CD80、PD-L2 和 CD73，我们发现，在原发性 PyNL 感染后长达 55 天和第二次 PyNL 感染后 4-6 天，CD80-PD-L2-CD73+B 细胞的频率增加。此外，将富集的免疫 CD19+CD73+B 细胞注入非免疫小鼠中，对 PyNL 感染的保护作用明显强于 CD73-B 细胞。有趣的是，这些 CD73+B 细胞中的很大一部分还表达 IgM 和 granzyme B，后者已越来越多地与抗疟保护性反应相关联。
