Modulation of airway inflammation by passive transfer of allergen-specificTh1 and Th2 cells in a mouse model of asthma

Although evidence is strong that Th cells play a major role in mediating th e airway inflammation observed in asthma, the relative contributions of the Th cell subsets, Th1 and Th2, are unclear. It has been suggested that asth ma is driven by Th2 predominant responses in the lung, but other data sugge st a role for Th1 cells as well. Here we show by intracellular cytokine sta ining and flow cytometric analysis that in the murine model of OVA-induced airway inflammation, both Th1 and Th2 cells are recruited to the airways. T h1 cells predominate early in the response and Th2 cells predominate late. We further show that increasing the number of Th1 cells by passive transfer of OVA-specific Th1 cells results in increased inflammation. This effect i s observed regardless of whether the T cells are transferred before sensiti zation or after airway inflammation is already in progress. Transfer of Th1 cells also results in increased recruitment of host T cells of both Th1 an d Th2 phenotypes, Passive transfer of Th2 cells results in little change in the inflammatory response. These results demonstrate that Ag-specific Th1 cells are not protective in this model of asthma, but rather may potentiate the inflammatory response.