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. 2020 Dec 11;11:552613. doi: 10.3389/fimmu.2020.552613

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Copyright © 2020 Dong

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Immune cells and signaling pathways implicated in type 2 immune response in carbon nanotube (CNT)-exposed lungs. Type 2 alarmin IL-33 is induced and activates mast cells, leading to increased secretion of type 2 cytokine IL-5 and recruitment of eosinophils, in CNT-exposed lungs. CNTs induce the differentiation of Th2 cells and the activation of STAT6 and GATA-3 in Th2 cells, resulting in the expression and secretion of type 2 cytokines IL-4 and IL-13, in the lung. Furthermore, the polarization of M2 macrophages is induced by CNTs in the lung. M2 macrophages exhibit STAT6 activation and produce various type 2 mediators, which function in suppressing acute inflammation, developing type 2 inflammation and chronic inflammation, and promoting lung fibrosis.