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Published ahead of print on April 17, 2003, doi:10.1165/rcmb.2003-0008OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 3, September 2003, 405-409

A more recent version of this article appeared on September 1, 2003
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Submitted on January 10, 2003
Revised on April 17, 2003

Accelerated airway dendritic cell maturation, trafficking and elimination in a mouse model of asthma

Karim Y Vermaelen1* and Romain A Pauwels1

1 Respiratory Diseases, Ghent University Hospital, Ghent, Belgium

* To whom correspondence should be addressed. E-mail: Karim.Vermaelen{at}rug.ac.be.

Pulmonary dendritic cells can induce both tolerogenic as well as inflammatory immune responses in the lung. Conversely, little is known about the impact of ongoing airway inflammation on pulmonary DC biology. In non-inflammatory conditions, expression of T-cell costimulatory molecules on mouse airway DCs is low and only upregulated after homing into draining thoracic lymph nodes. In this study, we reveal that ongoing allergic airway inflammation induces a premature upregulation of the T-cell costimulatory molecules CD40, B7-2 and ICAM-1 on DCs still present in the airways. In contrast, high surface expression of ICOS-L (Inducible COStimulator-Ligand, involved in respiratory tolerance induction) is restricted to DCs from non-inflamed lungs. In addition, during inflammation the migratory flux of allergen-transporting airway DCs towards draining thoracic nodes increases both in amplitude as well as in speed. Remarkably, migratory DCs from inflamed airways are short-lived in the draining lymph nodes, a finding that is temporally associated with a marked loss of the anti-apoptotic protein Bcl-2 in these cells. This study demonstrates the profound effects of ongoing allergen-driven airway inflammation on the dynamics of pulmonary dendritic cell physiology, a knowledge that could be exploited in the development of novel DC-based immunotherapies.




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