SLy2‐deficiency promotes B‐1 cell immunity and triggers enhanced production of IgM and IgG2 antibodies against pneumococcal vaccine,Immunity, Inflammation and Disease

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SLy2‐deficiency promotes B‐1 cell immunity and triggers enhanced production of IgM and IgG2 antibodies against pneumococcal vaccine
Immunity, Inflammation and Disease ( IF 3.1 ) Pub Date : 2020-10-24 , DOI: 10.1002/iid3.365
Jennifer Jaufmann ₁ , Leyla Tümen ₁ , Fee Schmitt ₁ , Daniel Schäll ₁ , Max von Holleben ₂ , Sandra Beer-Hammer _{1,

2}

Affiliation

Despite the benefits of existing vaccines, Streptococcus pneumoniae is still responsible for the greatest proportion of respiratory tract infections around the globe, thereby substantially contributing to morbidity and mortality in humans. B‐1 cells are key players of bacterial clearance during pneumococcal infection and even provide long‐lasting immunity towards S. pneumoniae. Previous reports strongly suggest an essential role of the immunoinhibitory adapter Src homology domain 3 lymphocyte protein 2 (SLy2) for B‐1 cell‐mediated antibody production. The objective of this study is to evaluate S. pneumoniae‐directed B cell responses in the context of SLy2 deficiency.

中文翻译：

SLy2 缺陷促进 B-1 细胞免疫并引发针对肺炎球菌疫苗的 IgM 和 IgG2 抗体的产生增强

尽管现有疫苗有好处，但肺炎链球菌仍然是全球呼吸道感染的最大原因，从而大大增加了人类的发病率和死亡率。B-1 细胞是肺炎球菌感染期间细菌清除的关键参与者，甚至提供对肺炎链球菌的持久免疫力。以前的报告强烈表明免疫抑制接头 Src 同源域 3 淋巴细胞蛋白 2 (SLy2) 对 B-1 细胞介导的抗体产生的重要作用。本研究的目的是在 SLy2 缺乏的情况下评估肺炎链球菌导向的 B 细胞反应。

更新日期：2020-11-12

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