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@ARTICLE{Knoll:163374,
author = {Knoll, Rainer and Schultze, Joachim L and
Schulte-Schrepping, Jonas},
title = {{M}onocytes and {M}acrophages in {COVID}-19.},
journal = {Frontiers in immunology},
volume = {12},
issn = {1664-3224},
address = {Lausanne},
publisher = {Frontiers Media},
reportid = {DZNE-2022-00137},
pages = {720109},
year = {2021},
note = {(CC BY)},
abstract = {COVID-19 is a contagious viral disease caused by SARS-CoV-2
that led to an ongoing pandemic with massive global health
and socioeconomic consequences. The disease is characterized
primarily, but not exclusively, by respiratory clinical
manifestations ranging from mild common cold symptoms,
including cough and fever, to severe respiratory distress
and multi-organ failure. Macrophages, a heterogeneous group
of yolk-sac derived, tissue-resident mononuclear phagocytes
of complex ontogeny present in all mammalian organs, play
critical roles in developmental, homeostatic and host
defense processes with tissue-dependent plasticity. In case
of infection, they are responsible for early pathogen
recognition, initiation and resolution of inflammation, as
well as repair of tissue damage. Monocytes, bone-marrow
derived blood-resident phagocytes, are recruited under
pathological conditions such as viral infections to the
affected tissue to defend the organism against invading
pathogens and to aid in efficient resolution of
inflammation. Given their pivotal function in host defense
and the potential danger posed by their dysregulated
hyperinflammation, understanding monocyte and macrophage
phenotypes in COVID-19 is key for tackling the disease's
pathological mechanisms. Here, we outline current knowledge
on monocytes and macrophages in homeostasis and viral
infections and summarize concepts and key findings on their
role in COVID-19. While monocytes in the blood of patients
with moderate COVID-19 present with an inflammatory,
interferon-stimulated gene (ISG)-driven phenotype, cellular
dysfunction epitomized by loss of HLA-DR expression and
induction of S100 alarmin expression is their dominant
feature in severe disease. Pulmonary macrophages in COVID-19
derived from infiltrating inflammatory monocytes are in a
hyperactivated state resulting in a detrimental loop of
pro-inflammatory cytokine release and recruitment of
cytotoxic effector cells thereby exacerbating tissue damage
at the site of infection.},
subtyp = {Review Article},
keywords = {COVID-19: immunology / COVID-19: pathology / HLA-DR
Antigens: immunology / Humans / Inflammation: immunology /
Inflammation: pathology / Macrophages: immunology /
Macrophages: pathology / Monocytes: immunology / Monocytes:
pathology / SARS-CoV-2: immunology / Severity of Illness
Index / COVID-19 (Other) / SARS-CoV-2 (Other) / alveolar
macrophage (Other) / hyperinflammation (Other) / macrophage
(Other) / monocytes (Other) / scRNA-seq (Other) / viral
infection (Other) / HLA-DR Antigens (NLM Chemicals)},
cin = {AG Schultze / AG Aschenbrenner / PRECISE},
ddc = {610},
cid = {I:(DE-2719)1013038 / I:(DE-2719)5000082 /
I:(DE-2719)1013031},
pnm = {354 - Disease Prevention and Healthy Aging (POF4-354)},
pid = {G:(DE-HGF)POF4-354},
experiment = {EXP:(DE-2719)PRECISE-20190321},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34367190},
pmc = {pmc:PMC8335157},
doi = {10.3389/fimmu.2021.720109},
url = {https://pub.dzne.de/record/163374},
}