Immunoglobulin E blocking in severe asthma

Abstract

Asthma is a heterogeneous chronic inflammatory disease affecting lower respiratory airways of both children and adults. Patients with a confirmed diagnosis of asthma, who have addressed modifiable factors, and continue to be poorly controlled even with high doses of corticosteroids, are classified as severe asthma, which is associated with higher mortality and hospitalizations, as well as low quality of life, and higher costs of medical care. High, low, and mixed type 2 immunoinflammatory mechanisms have been identified, where immunoglobulin E is a prominent biomarker for early-onset asthma, and in late-onset, non-allergic asthma. Blocking immunoglobulin E indirectly decreases the expression of its high-affinity receptor, decreasing the production of type 2 cytokines, and inhibiting eosinophilic inflammation, as well as modulating type 2 inflammation. On the other hand, preclinical and clinical evidence supports the existence of close counter-regulation of high-affinity immunoglobulin E receptor and interferon pathways, and a possible mechanism of prevention of virus-induces exacerbations. The following review summarizes the long clinical experience of blocking immunoglobulin E in severe asthma.