Modulation of the CD141/DC-SIGN/CD1c Monocyte by the Airway Epithelium: a Dysregulated Mechanism in Chronic Inflammatory Lung Disorders?

Abstract

It has been suggested more than 20 years ago that epithelial cells (ECs) are the major culprit in some lung diseases including asthma. Although their role in chronic lung diseases is undoubtedly unquestionable, the mechanisms by which ECs orchestrate the immune response are far from being fully understood today. Besides the production of mucus, surfactant, and periciliary fluids which have an important innate immune protection [1-3], one of the mechanisms that has earned important recognition concerns the molecular crosstalk between ECs and immune cells such as monocytes and dendritic cells (DCs). However, questions have arisen on how the modulation induced by direct cell contact vs. soluble components can be dissected in vivo. Recently published aspects regarding the modulation of monocyte derived DCs (ModDCs) by ECs in humans obtained from in vitro and ex vivo studies will be commented on the forthcoming sections.