Atopic asthma is characterized by inflammatory responses of the airway and is associated with up-regulation of Th2 cytokines, notably IL-4 and IL-5. A recently described human cytokine, IL-13, is a potent in vitro modulator of various cell types, including monocytes, B cells, and endothelial cells. Similar to IL-4, it is also involved in the induction of IgE synthesis. However, the in vivo expression and function of IL-13 and its relation to disease remain to be defined. Using a segmental allergen challenge model, we have examined the in vivo expression of IL-13 in the bronchoalveolar lavage (BAL) cells of atopic patients. We found a significant enhancement of both IL-13 transcripts and secreted proteins in the allergen-challenged BAL compared with the saline-challenged control sites of asthmatic and rhinitic patients. In contrast, the expression of IL-13 transcripts was not detected in the BAL of two normal subjects challenged with the same dose of ragweed allergen. The cellular source of IL-13 mRNA was identified in the mononuclear cell fraction of the allergen-challenged BAL. The allergen-induced quantitative differences in the level of transcripts were confirmed by competitive PCR assays. These results suggest that the significant increase in IL-13 in the allergen-challenged BAL is primarily from the mononuclear cells and is involved in the regulation of allergen-induced late phase inflammatory responses.