Figure 1.

Mechanism of Antigen-Induced alarmin release and subsequent immune response leading to airway hyperresponsiveness. Illustration of antigens inducing the release of alarmins including thymic stromal lymphopoietin (TSLP), eotaxin, and interleukin-33 (IL-33). The antigens are detected by dendritic cells, which in turn activate T-helper type 2 (Th2) cells and innate lymphoid cells (ILC2). The Th2 cells release cytokines, including IL-4, which promotes the infiltration of eosinophils. These eosinophils bind to vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on endothelial cells, facilitating their migration to the site of inflammation guided by eotaxin. This process leads to airway hyperresponsiveness, characterized by inflammation, fibrosis, and collagen deposition.