Asthma is a major problem in public health and
common in industrialized and developed
countries; over the past two decades, its
prevalence, severity, and incidence have been
increasing. Allergic asthma responses are
mediated by CD4+ T cells polarized to a Th2 cell
phenotype. Type-2 cytokines, such as IL-4, IL-5 and IL-13, derive the pathological features of
asthma, with airway hyper-responsiveness and
eosinophilia, elevated IgE, excessive production
of mucus, and airway remodelling. The
immunopathogenesis of allergic asthma is
complex and multifactorial. Allergic inflammation
of the bronchial airways highlights the
pathogenesis. Many genetic risk factors including
inflammatory pathways, with polymorphisms of
IL-4, IL-10, IL-13, and CD14, have been described
but are not present in the majority of patients.
CD86+ B cells are the subpopulation of B cells that
secrete IgE, which correlates with the increased
total IgE seen in patients with severe fungal asthma
(Athari, 2013a).