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

• 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
• ISSN: 0022-1767; 1550-6606; 1550-6606
• DOI: 10.4049/jimmunol.1201200

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.