Regulatory T cells and T helper 17 cells in viral infection

• Published in: Scandinavian 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
• Language: English
• Published: England Wiley Subscription Services, Inc 01.05.2020
• Subjects: 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; T helper 17 cells (Th17 cells); regulatory T cells (Tregs); viral infection
• ISSN: 0300-9475; 1365-3083; 1365-3083
• DOI: 10.1111/sji.12873

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.