The DC subsets that express αE integrin (CD103) have been described to exert antagonistic functions, driving T cells towards either an inflammatory (Th1/Th17) or immunosuppressive phenotype (regulatory T cells - Treg). These functions depend on the tissue they reside and microenvironment factors or stimuli that this Antigen-presenting cell (APC) subpopulation receive. In this regard, immunoregulatory phenotype has been described in small subsets of CD103+ DCs from lung and intestinal mucosa. The function of this APC subpopulation in pulmonary Paracoccidioides brasiliensis infection is poorly described. Here, we showed that lung CD103+ DCs contribute to Treg differentiation in a pulmonary P. brasiliensis infection model, which was attributed to downregulation of costimulatory molecules analyzed in these APC subtypes 21 days post-infection. Overall, this data suggests that P. brasiliensis infection caused an immunosuppression that has also been observed in patients with the most severe form of Paracoccidioidomycosis (PCM) – a sickness caused by this fungus genus. Furthermore, these results open new perspectives for knowledge of the mechanisms that underlie the higher percentage of Treg cells found in peripheral blood of PCM patients.

已描述表达 αE 整合素 (CD103) 的 DC 亚群发挥拮抗作用，驱动 T 细胞趋向炎症 (Th1/Th17) 或免疫抑制表型（调节性 T 细胞 - Treg）。这些功能取决于它们所在的组织以及该抗原呈递细胞 (APC) 亚群接受的微环境因素或刺激。在这方面，免疫调节表型已在来自肺和肠粘膜的 CD103+ DC 的小亚群中得到描述。这种 APC 亚群在肺 Paracoccidioides brasiliensis 感染中的功能描述得很少。在这里，我们发现肺 CD103 + DCs 有助于肺 P. brasiliensis 感染模型中的 Treg 分化，这归因于感染后 21 天在这些 APC 亚型中分析的共刺激分子的下调。全面的，该数据表明，P. brasiliensis 感染引起了免疫抑制，在最严重的副球孢子菌病 (PCM) 患者中也观察到这种情况 - 一种由该真菌属引起的疾病。此外，这些结果为了解 PCM 患者外周血中 Treg 细胞百分比较高的机制开辟了新的视角。