CD11c+ cells are required for antigen-induced increase of mast cells in the lung

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...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2012-10, Vol.189 (8), p.3869-3877
Main Authors: Dahlin, Joakim S, Feinstein, Ricardo, Cui, Yue, Heyman, Birgitta, Hallgren, Jenny
Format: Article
Language:English
Subjects:
Animals
CD11c Antigen - biosynthesis
CD11c Antigen - genetics
CD11c Antigen - physiology
Cell Movement - immunology
Chemokines - biosynthesis
Chemokines - physiology
Diphtheria Toxin - administration & dosage
Female
Humans
Immunologi
Immunology
Leukocyte Count
Lung - cytology
Lung - immunology
Lung - metabolism
Lymphocyte Depletion
Male
Mast Cells - cytology
Mast Cells - immunology
Mast Cells - metabolism
Mice
Mice, Inbred BALB C
Mice, Transgenic
Respiratory Mucosa - cytology
Respiratory Mucosa - immunology
Respiratory Mucosa - metabolism
Stem Cells - cytology
Stem Cells - immunology
Stem Cells - metabolism
Up-Regulation - genetics
Up-Regulation - immunology
Vascular Cell Adhesion Molecule-1 - biosynthesis
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Summary: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.
ISSN:0022-1767
1550-6606
1550-6606
DOI:10.4049/jimmunol.1201200