Type-I IFNs regulate the protective response against pneumococcal infection in splenic marginal zone.

肺炎链球菌是人类细菌性肺炎的病原体。细菌细胞壁成分中含有衣壳多糖，在逃避宿主免疫反应中起着重要作用。这就是为什么针对衣壳多糖的抗体通过诱导补体系统的激活和巨噬细胞或树突状细胞的吞噬而对肺炎链球菌的感染具有保护作用。I型干扰素(IFN)是肺炎链球菌感染后产生的一种干扰素，可能对细菌感染起调节作用。然而，目前尚不清楚I型干扰素是否影响抗脾边缘带B细胞肺炎球菌壳多糖的抗体产生。本研究揭示了I型干扰素对边缘带B细胞产生肺炎链球菌衣壳多糖特异性IgM的影响

Streptococcus pneumoniae is a causative agent of bacterial pneumonia in human. The bacterial cell wall components contain the capsular polysaccharides which play an important role for evading the host immune responses. That is why the antibody specific for capsular polysaccharides is protective against S. pneumoniae infection by inducing the activation of complements system and phagocytosis by macrophages or dendritic cells. Type-I interferons (IFNs) were shown to be induced in response to S. pneumoniae infection, and possibly regulate the bacterial infection. However, it is not clear whether the type-I IFNs affect the antibody production against pneumococcalcapsular polysaccharides from splenic marginal zone B cells. This study revealed the effects of Type-I IFNs against marginal zone B cells for production of IgM specific for pneumococcal capsular polysaccharides