Dendritic cells (DCs) are antigen-presenting and play a critical role in linking the innate to the adaptive immune response [1, 30]. Immature dendritic cells (DC0) near the epithelial surface are activated directly by CS or dangerous signals generated from TD . Dendritic cells undergo a maturation process and migrate towards the local lymph nodes. Naïve, quiescent T cells cannot enter the lung parenchyma. But once activated by matured DC, they can move into the lung and differentiate into Th1, Th2, Th17, T-regulatory (Treg) and CD8+T cells, which are proliferated by themselves, in their corresponding cytokine environments [31, 32], e.g., in the presence of IL-12 secreted by M1 (as well as DC), naïve CD4+T cells (Th0) differentiate into T helper 1 (Th1) cells [33–35]. The Th1 cells secrete IFN-γ to up-regulate the polarization process from M0 to M1 [22, 36]. A multi-node positive feedback loop, M1→IL12→Th1→IFN-γ→M1, is thus formed. In contrast to Th1, Th2 is polarized from Th0 in the presence of IL-4. Th2 produces IL-13 and IL-4, release of which further enhances the production of IL-10 and TGF-β by M2. In the presence of TGF-β, Th0 cells differentiate into Treg, which secrete IL-10 [22, 36]. TGF-β and IL-6 (rather than IL-23) together induce Th17 differentiation, leading to the production of IL-17 [37–41]. While IL-17 acts on epithelial cells to recruit neutrophils to cause tissue damage further, the activated epithelial cells in TD secrete IL-6, forming a positive feedback loop, IL-6→Th17→IL-17→TD→IL-6 . Th17 cells also produce IL-21 for the differentiation of CD8+T cells from naïve CD8 cytotoxic T lymphocytes (T0) [37, 42]. While CD8+T cells produce IFN-γ to enhance the M1 inflammatory activities, they also release granzyme B and perforins, causing apoptosis/necrosis of targeted cells and leading to TD further . In addition, IL-6 can down-regulate the activation of Treg that secretes IL-10 to inhibit Th17 . Consequently, a positive feedback loop, IL-6┫Treg→IL-10 ┫Th17→IL-17→TD → IL-6, is formed.