Regulatory T cells and T helper 17 cells in viral infection

CD4+ T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4+ T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) an...

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Published inScandinavian journal of immunology Vol. 91; no. 5; pp. e12873 - n/a
Main Authors Wan, Zhikai, Zhou, Zhifeng, Liu, Yao, Lai, Yuhan, Luo, Yuan, Peng, Xiaoping, Zou, Wei
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.05.2020
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Abstract CD4+ T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4+ T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection.
AbstractList CD4+ T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4+ T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection.
CD4 T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4 T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection.
CD4+ T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4+ T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection.CD4+ T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4+ T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection.
CD4 + T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4 + T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection.
Author Lai, Yuhan
Peng, Xiaoping
Liu, Yao
Luo, Yuan
Zhou, Zhifeng
Zou, Wei
Wan, Zhikai
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  organization: the First Affiliated Hospital of Nanchang University
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Issue 5
Keywords T helper 17 cells (Th17 cells)
regulatory T cells (Tregs)
viral infection
Language English
License 2020 The Scandinavian Foundation for Immunology.
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Notes Funding information
This work was supported by the National Science Foundation of China (Nos. 81660279 and 81701629) (Wei Zou); the Jiangxi Department of Science and Technology (Nos. 20161ACB21016, 20171BCB23088 and 20181ACH80002) (Wei Zou); and the start‐up funding for the scholars studying and coming back from abroad from the Ministry of Education, China (No. 2015060020102070) (Wei Zou).
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PublicationTitle Scandinavian journal of immunology
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Snippet CD4+ T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4+ T cells...
CD4 + T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4 + T...
CD4 T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4 T cells...
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StartPage e12873
SubjectTerms Adaptive immunity
Animals
CD4 antigen
Cell Communication - immunology
Cell differentiation
Functional plasticity
Helper cells
Hepatitis
Hepatitis B
Hepatitis C
HIV
Host-Pathogen Interactions - immunology
Human immunodeficiency virus
Humans
Immunomodulation
Immunoregulation
Infections
Lymphocyte Activation - immunology
Lymphocyte Count
Lymphocytes
Lymphocytes T
regulatory T cells (Tregs)
Respiratory syncytial virus
Signal Transduction
T helper 17 cells (Th17 cells)
T-Lymphocyte Subsets - immunology
T-Lymphocyte Subsets - metabolism
T-Lymphocytes, Regulatory - immunology
T-Lymphocytes, Regulatory - metabolism
Th17 Cells - immunology
Th17 Cells - metabolism
viral infection
Viral infections
Virus Diseases - immunology
Virus Diseases - metabolism
Virus Diseases - virology
Title Regulatory T cells and T helper 17 cells in viral infection
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fsji.12873
https://www.ncbi.nlm.nih.gov/pubmed/32090360
https://www.proquest.com/docview/2394729240
https://www.proquest.com/docview/2363085989
Volume 91
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