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Blood, Vol. 95 No. 7 (April 1), 2000:
pp. 2337-2345
Transgenic expression of granulocyte-macrophage
colony-stimulating factor induces the differentiation and
activation of a novel dendritic cell population in the lung
Jun Wang,
Denis P. Snider,
Bryan R. Hewlett,
Nick W. Lukacs,
Jack Gauldie,
Hong Liang, and
Zhou Xing
From the Department of Pathology and Molecular Medicine and Division
of Infectious Diseases, Centre for Gene Therapeutics,
McMaster University, Hamilton, ON, Canada; and the Department of
Pathology, University of Michigan, Ann Arbor, MI.
The role of granulocyte-macrophage colony-stimulating factor
(GM-CSF) in the differentiation of dendritic cells (DCs) during pulmonary viral infection was investigated by using a mouse model of
GM-CSF transgene expression established with an adenoviral vector
(AdGM-CSF). GM-CSF gene transfer resulted in increased levels of GM-CSF
in the lung, which peaked at day 4 and remained increased up to day 19. A striking cellular response composed predominantly of macrophage-like
cells was observed in the lung receiving AdGM-CSF but not control
vector. By FACS analysis, the majority of these cells were identified
at an early time point as macrophages and later as mature/activated
myeloid DCs characterized by CD11bbright,
CD11cbright, MHC class IIbright, and
B7.1bright. In contrast, GM-CSF had a weak effect on a
small DC population that was found present in normal lung and was
characterized by CD11cbright and CD11blow. By
immunohistochemistry staining for MHC II, the majority of activated
antigen-presenting cells were localized to the airway epithelium and
peribronchial/perivascular areas in the lung. A concurrently enhanced
Th1 immune response was observed under these conditions. The number of
CD4 and CD8 T cells was markedly increased in the lung expressing
GM-CSF, accompanied by increased release of interferon (IFN) in the
lung. Furthermore, lymphocytes isolated from either lung parenchyma or
local draining lymph nodes of these mice but not the control mice
released large amounts of IFN on adenoviral antigen stimulation in
vitro. These findings reveal that GM-CSF promotes the differentiation
and activation of a myeloid DC population primarily by acting on
macrophages during pulmonary immune responses.
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