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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dahlin, Joakim S. Feinstein, Ricardo Hallgren, Jenny Cui, Yue Heyman, Birgitta
Description	Country affiliation: Sweden Author Affiliation: Dahlin JS ( Department of Medical Biochemistry and Microbiology, Uppsala University, SE-751 23 Uppsala, Sweden.)
Abstract	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	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	8
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-10-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd11c Physiology Cell Movement Immunology Lung Cytology Mast Cells Up-regulation Animals Biosynthesis Genetics Chemokines Diphtheria Toxin Administration & Dosage Leukocyte Count Metabolism Lymphocyte Depletion Mice Mice, Inbred Balb C Mice, Transgenic Respiratory Mucosa Stem Cells Vascular Cell Adhesion Molecule-1 Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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