ABSTRACT
The worldwide prevalence and severity of allergic asthma have increased dramatically in recent decades. Therapeutic advances have unfortunately not kept pace, and asthma morbidity and mortality continue to rise. The cardinal features of allergic asthma include airway hyperresponsiveness (AHR) to a variety of specific and nonspecific stimuli, excessive airway mucus production, pulmonary eosinophilia, and elevated concentrations of serum immunoglobulin E (IgE). Although asthma is multifactorial in origin, it is generally accepted that it arises as a result of inappropriate immunological responses to common environmental antigens in genetically susceptible individuals (1). Specifically, a multitude of evidence suggests that CD4 T cells producing Th2 cytokines (IL-4, IL-5, IL-13) play a pivotal role in disease pathogenesis. Although extensive research is ongoing into the processes underlying the development of deleterious immune responses to the ubiquitous, otherwise harmless, antigens that drive the expression of allergic asthma, these mechanisms remain a mystery.
