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Human Lung Mononuclear Phagocytes in Health and Disease
#MMPMID28507549
Baharom F
; Rankin G
; Blomberg A
; Smed-Sörensen A
Front Immunol
2017[]; 8
(?): 499
PMID28507549
show ga
The lungs are vulnerable to attack by respiratory insults such as toxins,
allergens, and pathogens, given their continuous exposure to the air we breathe.
Our immune system has evolved to provide protection against an array of potential
threats without causing collateral damage to the lung tissue. In order to swiftly
detect invading pathogens, monocytes, macrophages, and dendritic cells
(DCs)-together termed mononuclear phagocytes (MNPs)-line the respiratory tract
with the key task of surveying the lung microenvironment in order to discriminate
between harmless and harmful antigens and initiate immune responses when
necessary. Each cell type excels at specific tasks: monocytes produce large
amounts of cytokines, macrophages are highly phagocytic, whereas DCs excel at
activating naïve T cells. Extensive studies in murine models have established a
division of labor between the different populations of MNPs at steady state and
during infection or inflammation. However, a translation of important findings in
mice is only beginning to be explored in humans, given the challenge of working
with rare cells in inaccessible human tissues. Important progress has been made
in recent years on the phenotype and function of human lung MNPs. In addition to
a substantial population of alveolar macrophages, three subsets of DCs have been
identified in the human airways at steady state. More recently, monocyte-derived
cells have also been described in healthy human lungs. Depending on the source of
samples, such as lung tissue resections or bronchoalveolar lavage, the specific
subsets of MNPs recovered may differ. This review provides an update on existing
studies investigating human respiratory MNP populations during health and
disease. Often, inflammatory MNPs are found to accumulate in the lungs of
patients with pulmonary conditions. In respiratory infections or inflammatory
diseases, this may contribute to disease severity, but in cancer patients this
may improve clinical outcomes. By expanding on this knowledge, specific lung MNPs
may be targeted or modulated in order to attain favorable responses that can
improve preventive or treatment strategies against respiratory infections, lung
cancer, or lung inflammatory diseases.
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