肺动脉高压
缺氧(环境)
医学
心脏病学
化学
内科学
氧气
有机化学
作者
Claudia Mickael,Linda Sanders,Michael H. Lee,Rahul Kumar,Dara C. Fonseca‐Balladares,Aneta Gandjeva,Kelly M. Cautivo,Biruk Kassa,Sushil Kumar,David Irwin,Delaney Swindle,Tzu Phang,Robert S. Stearman,Ari B. Molofsky,Amy S. McKee,Kurt R. Stenmark,Brian B. Graham,Rubin M. Tuder
标识
DOI:10.1096/fj.202400338rr
摘要
Pulmonary hypertension (PH) is a chronic and progressive disease with significant morbidity and mortality. It is characterized by remodeled pulmonary vessels associated with perivascular and intravascular accumulation of inflammatory cells. Although there is compelling evidence that bone marrow-derived cells, such as macrophages and T cells, cluster in the vicinity of pulmonary vascular lesions in humans and contribute to PH development in different animal models, the role of dendritic cells in PH is less clear. Dendritic cells' involvement in PH is likely since they are responsible for coordinating innate and adaptive immune responses. We hypothesized that dendritic cells drive hypoxic PH. We demonstrate that a classical dendritic cell (cDC) subset (cDC2) is increased and activated in wild-type mouse lungs after hypoxia exposure. We observe significant protection after the depletion of cDCs in ZBTB46 DTR chimera mice before hypoxia exposure and after established hypoxic PH. In addition, we find that cDC depletion is associated with a reduced number of two macrophage subsets in the lung (FolR2
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