Burkholderia cenocepacia is an emerging opportunistic pathogen for people with cystic fibrosis and chronic granulomatous disease. Intracellular survival in macrophages within a membrane-bound vacuole (BcCV) that delays acidification and maturation into lysosomes is a hallmark of B. cenocepacia infection. Intracellular B. cenocepacia induce an inflammatory response leading to macrophage cell death by pyroptosis through the secretion of a bacterial deamidase that results in the activation of the pyrin inflammasome. However, how or whether infected macrophages can process and present B. cenocepacia antigens to activate T-cells has not been explored. Engulfed bacterial protein antigens are cleaved into small peptides in the late endosomal major histocompatibility class II complex (MHC) compartment (MIIC). Here, we demonstrate that BcCVs and MIICs have overlapping features and that interferon-gamma-activated macrophages infected with B. cenocepacia can process bacterial antigens for presentation by class II MHC molecules to CD4⁺ T-cells and by class I MHC molecules to CD8⁺ T-cells. Infected macrophages also release processed bacterial peptides into the extracellular medium, stabilizing empty class I MHC molecules of bystander cells. Together, we conclude that BcCVs acquire MIIC characteristics, supporting the notion that macrophages infected with B. cenocepacia contribute to establishing an adaptive immune response against the pathogen.

Burkholderia cenocepacia是囊性纤维化和慢性肉芽肿病患者的一种新兴机会病原体。膜结合的液泡（BcCV）内的巨噬细胞中的细胞内存活会延迟酸化和成熟到溶酶体中，这是高新芽孢杆菌感染的标志。细胞内的新脓单胞菌通过细菌脱酰胺酶的分泌诱导发炎反应，从而通过热解作用导致巨噬细胞死亡，所述细菌脱酰胺酶导致活化了发炎的炎症小体。然而，尚未探索感染巨噬细胞如何或是否可以加工和呈递新酒双歧杆菌抗原以激活T细胞。吞噬的细菌蛋白抗原在后期的内体主要组织相容性II类复合物（MHC）区室（MIIC）中裂解为小肽。这里，⁺ T细胞，并按I类MHC分子转移至CD8 ⁺ T细胞。感染的巨噬细胞还将释放的细菌肽释放到细胞外培养基中，稳定旁观者细胞的空I类MHC分子。在一起，我们得出的结论是，BcCV具有MIIC特性，支持以下观念：感染了新细菌的巨噬细胞有助于建立针对病原体的适应性免疫应答。