Urban particulate matter (UPM) air pollution and vitamin D deficiency are detrimentally associated with respiratory health. This is hypothesized to be due in part to regulation of IL-17A, which UPM is reported to promote. Here, we used a myeloid dendritic cell (DC)-memory CD41 T cell co-culture system to characterize UPM-driven IL-17A 1 cells, investigate the mechanism by which UPM-primed DCs promote this phenotype, and address evidence for crossregulation by vitamin D.
Clinical RelevanceUrban particulate matter air pollution and vitamin D deficiency are both detrimentally associated with airway function. This research describes an IL-23-dependent pathway by which urban particulate matter promotes a proinflammatory T helper 17 cell response, which is predicted to exacerbate respiratory diseases, and the capacity of vitamin D to oppose this effect. This supports the concept that restoring vitamin D sufficiency will help to counteract the detrimental properties of air pollution to maintain immune homeostasis.