To test the roles of Th1 and Th2 cells in allergic airway hypersensitivity, we identified these cells in the airways of ovalbumin (OVA) sensitized and challenged mice using intracellular (i.e.) cytokine staining and FACS. We also tested the ability of passively transferred OVA-specific Th1 and Th2 cells from DO11.10 TCR transgenic mice to modulate the inflammatory response, using the anti-clonotypic mAb KJ1-26 to distinguish transferred from endogenous T cells. Mice sensitized i.p. with OVA then challenged with an OVA aerosol showed accumulation of both Th1 (IFN-γ+ by FACS) and Th2 (IL-4+ or IL-5+) cells as well as eosinophils in the airways. When DO11 Th1 cells were infused prior to sensitization, there was dramatically increased airway inflammation with substantial eosinophilia, and increased numbers of both the endogenous and the transferred DO11 Th1 cells. Endogenous Th2 cells were not reduced. When DO11 Th2 cells were infused prior to sensitization, challenge elicited increased numbers of endogenous Th2 cells, but no overall increase in inflammatory cells or eosinophils. Transferred transgenic Th1 and Th2 cells were both phenotypically stable in vivo. These data indicate that passively transferred Th1 cells do not block the accumulation of endogenous Th2 cells in the lung, but rather increase lung inflammation in this mouse model of allergic asthma. In addition, increasing the numbers of Th2 cells by passive transfer does not lead to increased eosinophilia or total inflammation.