Cardiovascular Research Institute, University of California, San Francisco, San Francisco, United States; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, United States; Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, United States
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, United States; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, United States
Cynthia Cho
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, United States; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, United States
Ross J Metzger
Department of Anatomy, University of California, San Francisco, San Francisco, United States
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, United States; Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, United States; Department of Anatomy, University of California, San Francisco, San Francisco, United States
In allergic asthma, allergen inhalation leads to local Th2 cell activation and peribronchial inflammation. However, the mechanisms for local antigen capture and presentation remain unclear. By two-photon microscopy of the mouse lung, we established that soluble antigens in the bronchial airway lumen were efficiently captured and presented by a population of CD11c+ interstitial macrophages with high CX3CR1-GFP and MHC class II expression. We refer to these cells as Bronchus-Associated Macrophages (BAMs) based on their localization underneath the bronchial epithelium. BAMs were enriched in collagen-rich regions near some airway branchpoints, where inhaled antigens are likely to deposit. BAMs engaged in extended interactions with effector Th2 cells and promoted Th2 cytokine production. BAMs were also often in contact with dendritic cells (DCs). After exposure to inflammatory stimuli, DCs migrated to draining lymph nodes, whereas BAMs remained lung resident. We propose that BAMs act as local antigen presenting cells in the lung and also transfer antigen to DCs.
