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Interaction Between Adaptive and Innate Immune Pathways in the Pathogenesis of Atopic Asthma: Operation of a Lung/Bone Marrow Axis

Patrick G. Holt, DSc; Peter D. Sly, DSc; for the CAMP Research Group
Author and Funding Information

From the Telethon Institute for Child Health Research and the Centre for Child Health Research (Dr Holt), The University of Western Australia, Perth, WA; and the Queensland Children’s Medical Research Institute and University of Queensland (Dr Sly), Brisbane, QLD, Australia.

Correspondence to: Patrick G. Holt, DSc, Division of Cell Biology, Telethon Institute for Child Health Research, Centre for Child Health Research, The University of Western Australia, PO Box 855, West Perth, WA 6872, Australia; e-mail: patrick@ichr.uwa.edu.au


Funding/Support: The authors are supported by the National Health and Medical Research Council of Australia.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;139(5):1165-1171. doi:10.1378/chest.10-2397
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Atopic asthma is the most common form of asthma, particularly during childhood, and in many cases it persists into adult life. Although atopy is clearly a risk factor for development of this disease, only a small subset of subjects sensitized to aeroallergens express persistent symptoms, suggesting that additional pathogenic mechanisms are involved. Recent studies have implicated respiratory viral infections as key cofactors in asthma development in atopic patients. In relation to initial expression of the asthma phenotype in early childhood, it has been shown that although both atopic sensitization and early severe lower respiratory tract infections can operate as independent asthma risk factors, the persistence of asthma is most frequent among children who experience both insults, suggesting that the relevant inflammatory pathways interact to maximally drive disease pathogenesis. Importantly, it has been established that both these factors must be operative contemporaneously for these interactions to occur (ie, the interactions are likely to be direct). Recent studies on viral-induced asthma exacerbations in atopic children have provided a plausible mechanism for these interactions. Notably, it has been demonstrated that signals triggered during the innate immune response to the virus can lead to the release of large numbers of migrating high-affinity IgE receptor-bearing bone marrow-derived precursors of mucosal dendritic cells into the blood. The subsequent trafficking of these cells to the infected airway mucosa where dendritic cell turnover is very high provides a potential mechanism for recruitment of underlying aeroallergen-specific T-helper 2 immunity into the already inflamed milieu in the infected airway mucosa.

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