Inflammation is a tissue response to a variety of harmful stimuli, such as pathogens, irritants, and
injuries, and can eliminate insults and limit tissue damage. However, dysregulated
inflammation is recognized as a cause of many human diseases, exemplified by organ
fibrosis and
cancer. In this regard,
inflammation-promoted
fibrosis is commonly observed in human
lung diseases, such as
idiopathic pulmonary fibrosis and
pneumoconiosis.
Carbon nanotubes (CNTs) are a type of nanomaterials with unique properties and various industrial and commercial applications. On the other hand, certain forms of CNTs are potent inducers of
inflammation and
fibrosis in animal lungs. Notably, acute
inflammation is a remarkable phenotype elicited by CNTs in the lung during the early acute phase post-exposure; whereas a type 2 immune response is evidently activated and dominates during the late acute and chronic phases, leading to type 2
inflammation and lung
fibrosis. Numerous studies demonstrate that these immune responses involve distinct immune cells, various pathologic factors, and specific functions and play crucial roles in the initiation and progression of
inflammation and
fibrosis in the lung exposed to CNTs. Thus, the mechanistic understanding of the immune responses activated by CNTs has drawn great attention in recent years. This article reviews the major findings on the cell signaling pathways that are activated in immune cells and exert functions in promoting immune responses in CNT-exposed lungs, which would provide new insights into the understanding of CNT-induced
lung inflammation and
inflammation-driven
fibrosis, the application of CNT-induced
lung inflammation and
fibrosis as a new disease model, and the potential of targeting immune cells as a therapeutic strategy for relevant human
lung diseases.