TY - JOUR
T1 - Neutrophils and lymphopenia, an unknown axis in severe COVID-19 disease
AU - Peñaloza, Hernán F.
AU - Lee, Janet S.
AU - Ray, Prabir
N1 - Funding Information:
This work was supported in part by the University of Pittsburgh Vascular Medicine Institute, the Hemophilia Center of Western Pennsylvania, and the Institute for Transfusion Medicine (H.F.P.) (https://www.vmi.pitt.edu/) and the National Heart, Lung, And Blood Institute of the National Institutes of Health (https://www.nhlbi.nih. gov/) under Award Numbers P01 HL114453 (P.R., J.S.L), R01 HL136143, R01 HL142084, K24 HL143285 (J.S.L.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or any other sponsoring agency. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Publisher Copyright:
© 2021 Peñaloza et al.
PY - 2021/9
Y1 - 2021/9
N2 - The Coronavirus Disease 2019 (COVID-19) is caused by the betacoronavirus Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) virus that can mediate asymptomatic or fatal infections characterized by pneumonia, acute respiratory distress syndrome (ARDS), and multi-organ failure. Several studies have highlighted the importance of B and T lymphocytes, given that neutralizing antibodies and T cell responses are required for an effective immunity. In addition, other reports have described myeloid cells such as macrophages and monocytes play a major role in the immunity against SARS-CoV-2 as well as dysregulated pro-inflammatory signature that characterizes severe COVID-19. During COVID-19, neutrophils have been defined as a heterogeneous group of cells, functionally linked to severe inflammation and thrombosis triggered by degranulation and NETosis, but also to suppressive phenotypes. The physiological role of suppressive neutrophils during COVID-19 and their implications in severe disease have been poorly studied and is not well understood. Here, we discuss the current evidence regarding the role of neutrophils with suppressive properties such as granulocytic myeloid-derived suppressor cells (G-MDSCs) and their possible role in suppressing CD4+ and CD8+ T lymphocytes expansion and giving rise to lymphopenia in severe COVID-19 infection.
AB - The Coronavirus Disease 2019 (COVID-19) is caused by the betacoronavirus Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) virus that can mediate asymptomatic or fatal infections characterized by pneumonia, acute respiratory distress syndrome (ARDS), and multi-organ failure. Several studies have highlighted the importance of B and T lymphocytes, given that neutralizing antibodies and T cell responses are required for an effective immunity. In addition, other reports have described myeloid cells such as macrophages and monocytes play a major role in the immunity against SARS-CoV-2 as well as dysregulated pro-inflammatory signature that characterizes severe COVID-19. During COVID-19, neutrophils have been defined as a heterogeneous group of cells, functionally linked to severe inflammation and thrombosis triggered by degranulation and NETosis, but also to suppressive phenotypes. The physiological role of suppressive neutrophils during COVID-19 and their implications in severe disease have been poorly studied and is not well understood. Here, we discuss the current evidence regarding the role of neutrophils with suppressive properties such as granulocytic myeloid-derived suppressor cells (G-MDSCs) and their possible role in suppressing CD4+ and CD8+ T lymphocytes expansion and giving rise to lymphopenia in severe COVID-19 infection.
UR - http://www.scopus.com/inward/record.url?scp=85115451077&partnerID=8YFLogxK
U2 - 10.1371/journal.ppat.1009850
DO - 10.1371/journal.ppat.1009850
M3 - Review article
C2 - 34473802
AN - SCOPUS:85115451077
SN - 1553-7366
VL - 17
JO - PLoS pathogens
JF - PLoS pathogens
IS - 9
M1 - 1009850
ER -