Figure 2.

Pathophysiological mechanisms of asthma that may act as facilitators of respiratory viral infections. (1) An impaired production of type I interferons (IFN‐α/IFN‐β) has been found in a high proportion of asthmatic patients. One of the mechanisms involves crosslinking of IgE bound to the high‐affinity receptor of IgE (FcεRI) by allergens in plasmacytoid dendritic cells (pDCs) that result in decreased toll‐like receptor (TLR) expression and a decline in type I interferons production. (2) T helper 2 (Th2) inflammation in asthma linked to the production of IL‐4, IL‐5 and IL‐13 by Th2 cells and group 2 innate lymphoid cells (ILC2s) has been related to reduced protection against viruses. Furthermore, allergen exposure can induce production in the epithelium of cytokines that can synergistically interact with respiratory viruses. (3) Asthma is characterized by abundant infiltration of immune cells that can act as infective targets for respiratory viruses. (4) In the context of Th2 polarization in atopic asthma, high amounts of specific IgE against different allergens are produced. Recent studies have proposed that specific IgE against certain viruses can also be produced.