Published ahead of print on November 22, 2006, doi:10.1165/rcmb.2006-0330OC Am. J. Respir. Cell Mol. Biol., Volume 36, Number 4, April 2007, 435-441 A more recent version of this article appeared on April 1, 2007
Submitted on September 3, 2006 Long-term Deposition of Inhaled Antigen in Lung Resident CD11b-CD11c+ CellsKate E Matthews1,1 Malaghan Institute of Medical Research, Wellington, New Zealand, 2 Department of Dermatology, DIAID, Medical University of Vienna, Vienna, Austria, 3 INSERM U503-IFR128, Lyon, France, 4 Department of Clinical Pathology, Medical University of Vienna, Vienna, Austria * To whom correspondence should be addressed. E-mail: fronchese{at}malaghan.org.nz.
In this study we report the characterization of a population of lung resident CD11b-CD11c+ cells that are able to take up inhaled antigen and retain it for extended periods of time. Ovalbumin conjugated to fluorescein-isothiocyanate (FITC-OVA) administered intranasally (i.n.) to mice was taken up by two main populations of cells in the lung, a migratory CD11c+CD11b+ population consisting of dendritic cells (DC), which rapidly transported antigen to the draining lymph node (LN), and a resident CD11b-CD11c+ population that retained engulfed antigen without apparently degrading it for up to 8 weeks after administration. The FITC+CD11b-CD11c+ cells did not migrate to draining LN at a detectable rate, and did not upregulate expression of costimulatory molecules in response to LPS treatment. FITC+CD11b-CD11c+ cells were found in the lung and broncho-alveolar lavage (BAL) fluid, and their distribution was compatible with macrophages. Although FITC+CD11b-CD11c+ cells expressed the DC marker DEC205 and other molecules associated with antigen presenting cell function, they did not induce proliferation of antigen-specific CD4+ T cells in vitro or acute cytokine production by activated CD4+ T cells in vivo. Thus, FITC+CD11b-CD11c+ cells appear to represent an intermediate cell type sharing properties with DC and macrophages. These cells may have a role in modulating the responses of lung resident T cells to inhaled antigens.
This article has been cited by other articles:
|
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||