Asthma has been strongly associated with a Th2-dominant immune response where Th2 cells produce interleukin 4 (IL-4) that, in turn, promotes the production of IgE by B cells that have undergone class switching following antigenic challenge (sensitization); however, the IgE immunoglobulin binds to receptors on mast cells, and following secondary exposure to the antigen, the mast cell releases histamine in an anti-helminthic response rather than an antiviral response [105]. Here, IGHE is linked to asthma.