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Editorial
. 2020 Jul 15;202(2):157-159.
doi: 10.1164/rccm.202003-0634ED.

Asthma and the Dysregulated Immune Response to Rhinovirus

Peter A B Wark  1   2
Affiliations
Editorial

Asthma and the Dysregulated Immune Response to Rhinovirus

Peter A B Wark. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
A proposed series of early-life events may predispose someone to develop asthma. Susceptible individuals in the first year of life display impaired type I and type II IFN responses (IRF7 lo), giving them an impaired antiviral immune phenotype. A viral infection leads to intense acute airway inflammation in the first year of life, resulting in bronchiolitis. Those with impaired immunity (IRF7 lo) have impaired IL-6 responses and are slower to clear the virus; they suffer more intense airway inflammation, and recurring infection develops with viruses such as rhinovirus-C (RV-C). The exaggerated airway inflammatory response continues and is now augmented by increased CCL-24, and airway eosinophilia develops. Reduced T-cell immune responses and recurring airway inflammation are associated with reduced T-regulatory (Treg) numbers and function, failing to control airway inflammation. In the airway, a cycle of damage and remodeling develops. Susceptible individuals develop sensitization to aeroallergens, especially dust mite. Type 2 airway inflammation becomes established. This in itself can predispose an individual to recurring RV infection that further exacerbates the impaired antiviral immunophenotype. Asthma is established, characterized by type 2 airway inflammation and recurring exacerbations triggered by RV-A and RV-C.
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Comment on

References

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Supplementary concepts