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Administration of interleukin‐12 exerts a therapeutic instead of a long‐term preventive effect on mite Der p I allergen‐induced animal model of airway inflammation

Interleukin‐12 (IL‐12) is a key cytokine, which promotes T helper type 1 (Th1) cell‐mediated immunity and inhibits Th2‐type responses. It has been previously shown that IL‐12 administration during active immunization following a single allergen exposure can prevent antigen‐induced increases in immunoglobulin E (IgE) formation, Th2 cytokine production and bronchoalveolar lavage (BAL) eosinophils in a murine model of allergic airway inflammation. Thus, these studies have now been extended and two IL‐12 treatment protocols on this murine model were evaluated. Administration of IL‐12 during the active immunization strikingly increased Der p I‐specific serum IgG2a and transiently decreased the levels of IgG1 and IgE antibodies following multiple allergen challenges. Such early treatment of IL‐12 down‐regulated IL‐5 production and modestly up‐regulated interferon‐γ production but did not effect BAL eosinophilia. These results suggest that repeated exposure to antigen and IL‐12 is necessary to maintain a persistent Th1‐recall response. Furthermore, administration of IL‐12 to actively immunized mice, in which Th2‐associated responses were established, had a significant effect on IgG2a synthesis and a modest effect on IgE levels, also down‐regulation of IL‐5 production, and markedly increased interferon‐γ production and abolished recruitment of eosinophils. Therefore, these data indicate that IL‐12 can inhibit antigen‐induced eosinophil infiltration into airways, despite the existence of a Th2‐associated response. Taken together, these studies suggest that IL‐12 may be useful as an immunotherapeutic agent in the treatment of such pulmonary allergic disorders as bronchial asthma.