Perspective of HLA-G Induced Immunosuppression in SARS-CoV-2 Infection

COVID-19, the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has threatened public health worldwide. Host antiviral immune responses are essential for viral clearance and disease control, however, remarkably decreased immune cell numbers and exhaustion of host cellul...

Full description

Bibliographic Details
Main Authors: Aifen Lin, Wei-Hua Yan
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-12-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2021.788769/full
_version_ 1818723546073923584
author Aifen Lin
Aifen Lin
Wei-Hua Yan
Wei-Hua Yan
author_facet Aifen Lin
Aifen Lin
Wei-Hua Yan
Wei-Hua Yan
author_sort Aifen Lin
collection DOAJ
description COVID-19, the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has threatened public health worldwide. Host antiviral immune responses are essential for viral clearance and disease control, however, remarkably decreased immune cell numbers and exhaustion of host cellular immune responses are commonly observed in patients with COVID-19. This is of concern as it is closely associated with disease severity and poor outcomes. Human leukocyte antigen-G (HLA-G) is a ligand for multiple immune inhibitory receptors, whose expression can be upregulated by viral infections. HLA-G/receptor signalling, such as engagement with immunoglobulin-like transcript 2 (ILT-2) or ILT-4, not only inhibit T and natural killer (NK) cell immune responses, dendritic cell (DC) maturation, and B cell antibody production. It also induces regulatory cells such as myeloid-derived suppressive cells (MDSCs), or M2 type macrophages. Moreover, HLA-G interaction with CD8 and killer inhibitory receptor (KIR) 2DL4 can provoke T cell apoptosis and NK cell senescence. In this context, HLA-G can induce profound immune suppression, which favours the escape of SARS-CoV-2 from immune attack. Although detailed knowledge on the clinical relevance of HLA-G in SARS-CoV-2 infection is limited, we herein review the immunopathological aspects of HLA-G/receptor signalling in SARS-CoV-2 infection, which could provide a better understanding of COVID-19 disease progression and identify potential immunointerventions to counteract SARS-CoV-2 infection.
first_indexed 2024-12-17T21:12:14Z
format Article
id doaj.art-8b59a77abbb145efbbef9165d057a418
institution Directory Open Access Journal
issn 1664-3224
language English
last_indexed 2024-12-17T21:12:14Z
publishDate 2021-12-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Immunology
spelling doaj.art-8b59a77abbb145efbbef9165d057a4182022-12-21T21:32:26ZengFrontiers Media S.A.Frontiers in Immunology1664-32242021-12-011210.3389/fimmu.2021.788769788769Perspective of HLA-G Induced Immunosuppression in SARS-CoV-2 InfectionAifen Lin0Aifen Lin1Wei-Hua Yan2Wei-Hua Yan3Biological Resource Center, Taizhou Hospital of Zhejiang Province, Wenzhou Medical University, Linhai, ChinaKey Laboratory of Minimally Invasive Techniques & Rapid Rehabilitation of Digestive System Tumor of Zhejiang Province, Taizhou Hospital of Zhejiang Province, Linhai, ChinaKey Laboratory of Minimally Invasive Techniques & Rapid Rehabilitation of Digestive System Tumor of Zhejiang Province, Taizhou Hospital of Zhejiang Province, Linhai, ChinaMedical Research Center, Taizhou Hospital of Zhejiang Province, Wenzhou Medical University, Linhai, ChinaCOVID-19, the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has threatened public health worldwide. Host antiviral immune responses are essential for viral clearance and disease control, however, remarkably decreased immune cell numbers and exhaustion of host cellular immune responses are commonly observed in patients with COVID-19. This is of concern as it is closely associated with disease severity and poor outcomes. Human leukocyte antigen-G (HLA-G) is a ligand for multiple immune inhibitory receptors, whose expression can be upregulated by viral infections. HLA-G/receptor signalling, such as engagement with immunoglobulin-like transcript 2 (ILT-2) or ILT-4, not only inhibit T and natural killer (NK) cell immune responses, dendritic cell (DC) maturation, and B cell antibody production. It also induces regulatory cells such as myeloid-derived suppressive cells (MDSCs), or M2 type macrophages. Moreover, HLA-G interaction with CD8 and killer inhibitory receptor (KIR) 2DL4 can provoke T cell apoptosis and NK cell senescence. In this context, HLA-G can induce profound immune suppression, which favours the escape of SARS-CoV-2 from immune attack. Although detailed knowledge on the clinical relevance of HLA-G in SARS-CoV-2 infection is limited, we herein review the immunopathological aspects of HLA-G/receptor signalling in SARS-CoV-2 infection, which could provide a better understanding of COVID-19 disease progression and identify potential immunointerventions to counteract SARS-CoV-2 infection.https://www.frontiersin.org/articles/10.3389/fimmu.2021.788769/fullHLA-Gimmune receptorSARS-CoV-2COVID-19immune suppression
spellingShingle Aifen Lin
Aifen Lin
Wei-Hua Yan
Wei-Hua Yan
Perspective of HLA-G Induced Immunosuppression in SARS-CoV-2 Infection
Frontiers in Immunology
HLA-G
immune receptor
SARS-CoV-2
COVID-19
immune suppression
title Perspective of HLA-G Induced Immunosuppression in SARS-CoV-2 Infection
title_full Perspective of HLA-G Induced Immunosuppression in SARS-CoV-2 Infection
title_fullStr Perspective of HLA-G Induced Immunosuppression in SARS-CoV-2 Infection
title_full_unstemmed Perspective of HLA-G Induced Immunosuppression in SARS-CoV-2 Infection
title_short Perspective of HLA-G Induced Immunosuppression in SARS-CoV-2 Infection
title_sort perspective of hla g induced immunosuppression in sars cov 2 infection
topic HLA-G
immune receptor
SARS-CoV-2
COVID-19
immune suppression
url https://www.frontiersin.org/articles/10.3389/fimmu.2021.788769/full
work_keys_str_mv AT aifenlin perspectiveofhlaginducedimmunosuppressioninsarscov2infection
AT aifenlin perspectiveofhlaginducedimmunosuppressioninsarscov2infection
AT weihuayan perspectiveofhlaginducedimmunosuppressioninsarscov2infection
AT weihuayan perspectiveofhlaginducedimmunosuppressioninsarscov2infection