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-Dependent Mechanism1
*
Asthma Research Group, Department of Medicine, McMaster University, Hamilton, Ontario, Canada; and
Department of Cell Biology and Immunology Faculty of Medicine, Vrije University, Amsterdam, The Netherlands
In the mucosal immune system, resident dendritic cells are
specialized for priming Th2-polarized immunity, whereas the
Ag-presenting activity of macrophages has been linked with the
development of Th1 phenotype. As an immune switch toward Th1 can
protect against Th2-mediated allergic response, this study investigated
the capacity of lung macrophages to stimulate Th1 responses during the
secondary exposure to inhaled allergen, thereby suppressing
Th2-mediated allergic airway inflammation in a murine model of allergic
asthma. Following airway macrophage depletion in OVA-sensitized mice,
lung T cells defaulted to a phenotype that produced less Th1 (IFN-
)
and more Th2 (IL-4 and IL-5) cytokines, leading to more severe airway
hyperreactivity and inflammation after intranasal Ag challenge. After
OVA pulsing and adoptive transfer, lung macrophages selectively
promoted a Th1 response in Ag-sensitized recipients and did not induce
pulmonary eosinophilia. By contrast, OVA pulsing and adoptive transfer
of a lung cell preparation, consisting of dendritic cells, B cells, and
macrophages, promoted a Th2 response with an associated inflammatory
response that was suppressed when macrophages were present and
pretreated with IFN-, but exacerbated when macrophages were depleted
before IFN- treatment. In addition, Th1-promoting activity of lung
macrophages was not related to the autocrine production of IL-12p40.
These results suggest that the Th1-promoting APC activity may be an
inherent property of the lung macrophage population, and may play an
important role, upon stimulation by IFN-, in antagonizing an ongoing
Th2 immunity and Th2-dependent allergic responses.
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