Mast cells are well recognized as key cells in allergic reactions, such as asthma and allergic airway diseases. However, the effects of mast cells and TNF-${alpha}$ on T-helper type 2 (Th2) cytokine-dependent asthma are not clearly understood. Therefore, an aim of this study was to investigate the role of mast cells on Th2 cytokine-dependent airway hyperresponsiveness and inflammation. We used genetically mast cell-deficient WBB6F1/J-$Kit^W$/$Kit^{W-v}$ ($W/W^v$), congenic normal WBB6F1/J-$Kit^+$/$Kit^+$ (+/+), and mast cell-reconstituted $W/W^v$ mouse models of allergic asthma to investigate the role of mast cells in Th2 cytokine-dependent asthma induced by ovalbumin (OVA). And we investigated whether the intratracheal injection of TNF-${alpha}$ directly induce the expression of ICAM-1 and VCAM-1 in $W/W^v$ mice. This study, with OVA-sensitized and OVA-challenged mice, revealed the following typical histopathologic features of allergic diseases: increased inflammatory cells of the airway, airway hyperresponsiveness, and increased levels of TNF-${alpha}$, intercellular adhesion molecule (ICAM)-1, and vascular cellular adhesion molecule (VCAM)-1. However, the histopathologic features and levels of ICAM-1 and VCAM-1 proteins in $W/W^v$ mice after OVA challenges were significantly inhibited. Moreover, mast cell-reconstituted $W/W^v$ mice showed restoration of histopathologic features and recovery of ICAM-1 and VCAM-1 protein levels that were similar to those found in +/+ mice. Intratracheal administration of TNF-${alpha}$ resulted in increased ICAM-1 and VCAM-1 protein levels in $W/W^v$ mice. These results suggest that mast cells play a key role in a Th2 cytokine-dependent asthma model through production of adhesion molecules, including ICAM-1 and VCAM-1, by liberation of TNF-${alpha}$.