I focused to identify the specific role of immune cells that include dendritic cells and T cells in the regulation of allergic airway inflammation and remodeling using animal models of allergy. Based on these experiences, I moved to the studies to define the molecules and signaling mechanisms directly associated with airway inflammation and remodeling after I started my postdoctoral training at Yale University. At beginning, I investigated the role of chitinases in the pathogenesis of interstitial lung disease. These studies identified that a significant role of Chitinase1 (Chit1) in the pathogenesis of pulmonary fibrosis by enhancing TGF-b receptor expression and signaling. Later, I focused to determine the role and signaling mechanism of Chi3l1, a Chitinase-like protein in the pathogenesis of lung inflammation, injury and remodeling. Recently, our group identified a receptor and its co-receptor IL-13R2 and transmembrane 219 (TMEM219), that binds and mediates the cellular and tissue effects Chi3l1 and IL- 13. These studies provide fundamental and novel mechanistic insights on the biological function of Chi3l1 associated with the pathogenesis of various human diseases including asthma and pulmonary fibrosis.