Asthma is one of the leading causes of childhood hospitalisation and its incidence is on the rise throughout the world. Currently, the standard treatment for asthma is the use of corticosteroids to try to suppress the inflammatory reaction taking place in the bronchial tree. Using a murine model of atopic allergic asthma employing a methacholine hyperresponsive (A/J) as well as a hyporesponsive (C57BL/6) strain of mice sensitised and challenged with ovalbumin, we show that treatment with a synthetic Toll-like receptor 7 ligand (S28463, a member of the imidazoquinoline family) prevents development of the asthmatic phenotype. Treatment with S28463 resulted in a reduction of airway resistance and elastance following ovalbumin sensitisation and challenge. This was accompanied by a dramatic reduction in infiltration of leukocytes, especially eosinophils, into the lungs of both C57BL/6 and A/J mice following OVA challenge. Treatment with S28463 also abolished both the elevation in serum IgE level as well as the induction of IL-4, IL-5 and IL-13 by OVA challenge. The protective effects of S28463 were also observed in MK2 knockout, but not MYD88 knockout mice. We did not observe a switch in cytokine profile from T_H2 to T_H1, as both IL-12p70 and IFN-gamma levels were reduced following S28463 treatment. These results clearly demonstrate the anti-inflammatory effect of imidazoquinolines in an allergic asthma model as well as the clinical potential of TLR7 ligands in the treatment of allergic diseases.