Conversely, mice deficient in IL-25 exhibit reduced TH2-type immune responses [120, 121] and blocking IL-25 by the use of a monoclonal antibody or by a soluble IL-25 receptor (sIL-25R) prevented from development of AHR, production of allergen-specific IgE, allergic airway inflammation, and increased mucus production in a mouse model of experimental asthma [122, 123]. The gene discussed is IGHE; the disease is asthma.