Critical Care Medicine Department, National Institutes of Health (NIH) Clinical Center, Bethesda.
Laboratory of Human Retrovirology and Immunoinformatics, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, Maryland.
J Infect Dis. 2018 Oct 5;218(10):1631-1640. doi: 10.1093/infdis/jiy342.
The major surface glycoprotein (Msg) is the most abundant surface protein among Pneumocystis species. Given that Msg is present on both the cyst and trophic forms of Pneumocystis and that dendritic cells play a critical role in initiating host immune responses, we undertook studies to examine activation of bone marrow-derived myeloid dendritic cells by Msg purified from Pneumocystis murina. Incubation of dendritic cells with Msg did not lead to increased expression of CD40, CD80, CD86, or major histocompatibility complex class II or to increased secretion of any of 10 cytokines. Microarray analysis identified very few differentially expressed genes. In contrast, lipopolysaccharide-activated dendritic cells had positive results of all of these assays. However, Msg did bind to mouse mannose macrophage receptor and human DC-SIGN, 2 C-type lectins expressed by dendritic cells that are important in recognition of pathogen-associated high-mannose glycoproteins. Deglycosylation of Msg demonstrated that this binding was dependent on glycosylation. These studies suggest that Pneumocystis has developed a mechanism to avoid activation of dendritic cells, potentially by the previously identified loss of genes that are responsible for the high level of protein mannosylation found in other fungi.
主要表面糖蛋白(Msg)是肺孢子菌属中最丰富的表面蛋白。鉴于 Msg 存在于肺孢子菌的囊和滋养形式上,并且树突状细胞在启动宿主免疫反应中起着关键作用,我们进行了研究,以检查从鼠肺孢子菌中纯化的 Msg 对骨髓来源的髓样树突状细胞的激活作用。树突状细胞与 Msg 孵育不会导致 CD40、CD80、CD86 或主要组织相容性复合物 II 的表达增加,也不会导致 10 种细胞因子中的任何一种分泌增加。微阵列分析仅鉴定出少数差异表达的基因。相比之下,脂多糖激活的树突状细胞在所有这些检测中均呈阳性结果。然而,Msg 确实与小鼠甘露糖巨噬细胞受体和人 DC-SIGN 结合,这两种 C 型凝集素由树突状细胞表达,在识别与病原体相关的高甘露糖糖蛋白方面非常重要。Msg 的去糖基化表明这种结合依赖于糖基化。这些研究表明,肺孢子菌已经开发出一种机制来避免树突状细胞的激活,可能是通过先前确定的丧失负责其他真菌中高水平蛋白甘露糖化的基因。