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Publication : Modulation of dendritic cell trafficking to and from the airways.

First Author  Jakubzick C Year  2006
Journal  J Immunol Volume  176
Issue  6 Pages  3578-84
PubMed ID  16517726 Mgi Jnum  J:129506
Mgi Id  MGI:3769597 Doi  10.4049/jimmunol.176.6.3578
Citation  Jakubzick C, et al. (2006) Modulation of dendritic cell trafficking to and from the airways. J Immunol 176(6):3578-84
abstractText  We investigated the fate of latex (LX) particles that were introduced into mice intranasally. Macrophages acquired the vast majority of particles and outnumbered LX particle-bearing airway dendritic cells (DCs) by at least two orders of magnitude. Yet alveolar macrophages were refractory to migration to the draining lymph node (DLN), and all transport to the DLN could be ascribed to the few LX(+) airway DCs. Upon macrophage depletion, markedly greater numbers of DCs were recruited into the alveolar space. Consequently, the number of DCs that carried particles to the DLN was boosted by 20-fold. Thus, a so far overlooked aspect of macrophage-mediated suppression of airway DC function stems from the modulation of DC recruitment into the airway. This increase in DC recruitment permitted the development of a robust assay to quantify the subsequent migration of DCs to the DLN. Therefore, we determined whether lung DCs use the same molecules that skin DCs use during migration to DLNs. Like skin DCs, lung DCs used CCR7 ligands and CCR8 for emigration to DLN, but the leukotriene C(4) transporter multidrug resistance-related protein 1 did not mediate lung DC migration as it does in skin, indicating that pathways governing DC migration from different tissues partially differ in molecular regulation.
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