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J Allergy Clin Immunol. 2008 Jul;122(1):69-77, 77.e1-2. doi: 10.1016/j.jaci.2008.03.028. Epub 2008 May 9.

Virus-induced eosinophil mediator release requires antigen-presenting and CD4+ T cells.

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Pulmonary Research Group, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.



The most frequent trigger of asthma exacerbation is infection with common airway viruses; however, the precise mechanism regulating such severe reactions is not understood. The presence of airway eosinophil products is a unique feature detected in asthmatic airways. Using an animal model, we previously demonstrated that T cells play an important role in regulating an eosinophil-dependant pathway of virus-induced airway hyperreactivity. We hypothesize that human eosinophils respond to viruses, although only after interaction with T cells.


We sought to determine whether eosinophils can respond to airway viruses in vitro and determine the mechanism of response.


An in vitro coculture model of human eosinophils, antigen-presenting cells, and T cells was used with parainfluenza virus, respiratory syncytial virus, or rhinovirus. We measured release of eosinophil peroxidase (EPO) in concert with T-cell proliferation, cytokine release, and changes in T-cell phenotype.


The viruses induced release of EPO when coincubated in the presence of antigen-presenting cells (dendritic cells or macrophages) and T cells. Virus-mediated release was associated with proliferation of CD3(+)CD4(+) T cells and release of cytokines. UV inactivation of the virus did not prevent virus-induced EPO release or T-cell proliferation. Proliferating CD4(+) T cells show increased expression of CD25 and CD45RO. CD8(+) T cells were not activated.


Virus-induced EPO release can occur in the context of antigen presentation to CD4(+) T cells.

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