Abstract
A proinflammatory role of T helper (Th)17 cells, producing IL-22 and IL-17A, has been favored although there is evidence for negative immune regulation by IL-17A. Here we show that IL-22 was produced during an allergic response in lungs of mice, immunized and challenged with ovalbumin (OVA), and that IL-22 neutralization further augmented the eosinophil recruitment to the lung. In a second allergy model, transfer of OVA-pulsed dendritic cells (DC) into naive mice conveyed eosinophil recruitment in response to subsequent inhaled OVA challenge, while DC preincubation with recombinant IL-22 abolished this response. Similarly, DC preincubation with IL-17A abolished DC-driven eosinophil recruitment, showing that both Th17 cytokines IL-22 and IL-17A mediate negative regulation of allergy by acting on DCs. Therefore, IL-22 inhibits DC functions and attenuates an allergic response.
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