Long-Term Deposition of Inhaled Antigen in Lung Resident CD11b−CD11c+ Cells
KE Matthews, A Karabeg, JM Roberts… - American journal of …, 2007 - atsjournals.org
KE Matthews, A Karabeg, JM Roberts, S Saeland, G Dekan, MM Epstein, F Ronchese
American journal of respiratory cell and molecular biology, 2007•atsjournals.orgIn 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
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 …
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
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 …
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 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 wk after administration. The FITC+CD11b−CD11c+ cells did not migrate to draining LN at a detectable rate, and did not up-regulate expression of costimulatory molecules in response to LPS treatment. FITC+CD11b−CD11c+ cells were found in the lung and bronchoalveolar lavage 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.
