Journal
JOURNAL OF IMMUNOLOGY
Volume 189, Issue 8, Pages 3869-3877Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1201200
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Funding
- Swedish Research Council
- Magnus Bergvall Foundation
- Bror Hjerpstedt Foundation
- Lars Hierta Memory Foundation
- Ellen, Walter, and Lennart Hesselman Foundation
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Patients with allergic asthma have more lung mast cells, which likely worsens the symptoms. In experimental asthma, CD11c(+) cells have to be present during the challenge phase for several features of allergic inflammation to occur. Whether CD11c(+) cells play a role for Ag-induced increases of lung mast cells is unknown. In this study, we used diphtheria toxin treatment of sensitized CD11c-diphtheria toxin receptor transgenic mice to deplete CD11c(+) cells. We demonstrate that recruitment of mast cell progenitors to the lung is substantially reduced when CD11c(+) cells are depleted during the challenge phase. This correlated with an impaired induction of endothelial VCAM-1 and led to a significantly reduced number of mature mast cells 1 wk after challenge. Collectively, these data suggest that Ag challenge stimulates CD11c(+) cells to produce cytokines and/or chemokines required for VCAM-1 upregulation on the lung endothelium, which in turn is crucial for the Ag-induced mast cell progenitor recruitment and the increase in mast cell numbers. The Journal of Immunology, 2012, 189: 3869-3877.
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