The third minireview also takes on certain aspects of allergic asthma. In particular, it focuses on elevated IgE levels and increased IgE sensitization as disease hallmarks. Genentech’s Lawren C. Wu notes that IgE binding to high-affinity FcεRI and the low-affinity FcεRII/CD23 receptors should be an important goal of future research. Additional points for investigation include “novel cell surface and intracellular mediators of FcεRI activation, mechanisms of intracellular calcium signaling, and new inhibitory proteins that negatively regulate parts of the signaling network downstream of FcεRI activation.”
Peter J. Barnes at Imperial College London covers signaling pathways of existing – and quite effective – therapies for asthma in the fourth minireview. Bronchodilators, like the β2-adrenergic receptor (β2AR) agonists, relax airway smooth muscle cells by increasing cyclic AMP concentrations and opening large conductance Ca2+ channels. Glucocorticoids are anti-inflammatory treatments that turn off multiple activated inflammatory genes. Beneficial molecular interactions between β2AR and glucocorticoid-activated pathways exist. Barnes says that our relatively good understanding of how current asthma therapies work in terms of their biochemical mechanisms will help to tweak existing treatments and invent new ones.
This thematic minireview series, like its predecessors, aims to link biochemical processes to an important clinical challenge. Over the past 50 years, both the incidence and the severity of asthma have increased globally, further burdening national public-health services. Still forthcoming in this thematic series are two minireviews, one on exercise-induced asthma by Lisa M. Schwiebert at the University of Alabama and the other on myeloid-derived regulatory cells and redox control in asthma by David D. Chaplin at the University of Alabama.
Visit this thematic series online at http://www.jbc.org/site/thematics/asthma.
Rajendrani Mukhopadhyay (firstname.lastname@example.org) is a senior science writer and editor for ASBMB.