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Huang, Ya-Xin; Zhao, Qiyi; Wu, Lili; Xie, Dongying; Gao, Zhiliang; Deng, Hong

doi:10.1155/2018/1020925

Cited by 6 publications

(4 citation statements)

References 38 publications

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“…However, in cHBV, IL-21 production in response to HBsAg peptides was decreased compared to acute infection [ 74 ]. Yet, an increased frequency of circulating Tfh was found and associated with HBeAg seroconversion as higher levels were detected in cHBV patients with HBeAg loss [ 74 , 75 , 76 ]. Furthermore, the Tfh from HBeAg seroconverters produced higher levels of IL-21 and harbored augmented frequencies of anti-HBe antibodies secreting B cells in vitro [ 75 ].…”

Section: Cd4 + T Cells In Chronic Hepatitis Bmentioning

confidence: 99%

CD4+ T Cells in Chronic Hepatitis B and T Cell-Directed Immunotherapy

Buschow

Jansen

2021

Cells

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The impaired T cell responses observed in chronic hepatitis B (HBV) patients are considered to contribute to the chronicity of the infection. Research on this impairment has been focused on CD8+ T cells because of their cytotoxic effector function; however, CD4+ T cells are crucial in the proper development of these long-lasting effector CD8+ T cells. In this review, we summarize what is known about CD4+ T cells in chronic HBV infection and discuss the importance and opportunities of including CD4+ T cells in T cell-directed immunotherapeutic strategies to cure chronic HBV.

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Section: Cd4 + T Cells In Chronic Hepatitis Bmentioning

confidence: 99%

CD4+ T Cells in Chronic Hepatitis B and T Cell-Directed Immunotherapy

Buschow

Jansen

2021

Cells

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“…In CHB patients, high expression of follicular helper T (Tfh) cell and CD4+ T cell C-X-C chemokine receptor type 5 (CXCR5) has been identified as positively correlated with immune activation. However, the understanding of the increased expression of chemokine receptors is limited (Huang et al, 2018). It has been shown that HBV infection does not affect the overall frequency of CD8 + CXCR5 + cells, while chronically infected patients accompanied with CD8 + CXCR5cells increased.…”

Section: Therapeutics That Modulate Chemokine Signaling Pathways To C...mentioning

confidence: 99%

Novel Molecular Therapeutics Targeting Signaling Pathway to Control Hepatitis B Viral Infection

Yan

Qiu

Davgadorj

et al. 2022

Front. Cell. Infect. Microbiol.

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Numerous canonical cellular signaling pathways modulate hepatitis B virus (HBV) replication. HBV genome products are known to play a significant role in regulating these cellular pathways for the liver’s viral-related pathology and physiology and have been identified as the main factor in hepatocarcinogenesis. Signaling changes during viral replication ultimately affect cellular persistence, multiplication, migration, genome instability, and genome damage, leading to proliferation, evasion of apoptosis, block of differentiation, and immortality. Recent studies have documented that numerous signaling pathway agonists or inhibitors play an important role in reducing HBV replication in vitro and in vivo, and some have been used in phase I or phase II clinical trials. These optional agents as molecular therapeutics target cellular pathways that could limit the replication and transcription of HBV or inhibit the secretion of the small surface antigen of HBV in a signaling-independent manner. As principle-based available information, a combined strategy including antiviral therapy and immunomodulation will be needed to control HBV infection effectively. In this review, we summarize recent findings on interventions of molecular regulators in viral replication and the interactions of HBV proteins with the components of the various targeting cellular pathways, which may assist in designing novel agents to modulate signaling pathways to prevent HBV replication or carcinogenesis.

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“…Thus, the function of MZP B cells in supporting the migration of Tfh cells through CCR7 needs further confirmation. Notably, cTfh cells with low CCR7 expression are increased and have been described as an indicator in autoimmune diseases including AIH ( 148 ) and pSS ( 125 ), as well as chronic HBV infection ( 149 ). CCR7 int Tfh cells in the blood are closest to tonsillar Tfh lineage cells and exhibit a more potent capacity to induce memory B cells to differentiate into antibody-producing cells than CCR7 high Tfh cells ( 150 ).…”

Section: Novel Insights Into Breg-mediated Regulation Of Tfh and Tfr In Autoantibody Productionmentioning

confidence: 99%

Frontiers of Autoantibodies in Autoimmune Disorders: Crosstalk Between Tfh/Tfr and Regulatory B Cells

Ding

et al. 2021

Front. Immunol.

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Balance of Tfh/Tfr cell is critically important for the maintenance of immune tolerance, as evidenced by the fact that T follicular helper (Tfh) cells are central to the autoantibodies generation through providing necessary help for germinal center (GC) B cells, whereas T follicular regulatory (Tfr) cells significantly inhibit autoimmune inflammation process through restraining Tfh cell responses. However, signals underlying the regulation of Tfh and Tfr cells are largely undefined. Regulatory B cells (Bregs) is a heterogeneous subpopulation of B cells with immunosuppressive function. Considerable advances have been made in their functions to produce anti‐inflammatory cytokines and to regulate Th17, Th1, and Treg cells in autoimmune diseases. The recent identification of their correlations with dysregulated Tfr/Tfh cells and autoantibody production makes Bregs an important checkpoint in GC response. Bregs exert profound impacts on the differentiation, function, and distribution of Tfh and Tfr cells in the immune microenvironment. Thus, unraveling mechanistic information on Tfh-Breg and Tfr-Breg interactions will inspire novel implications for the establishment of homeostasis and prevention of autoantibodies in diverse diseases. This review summarizes the dysregulation of Tfh/Tfr cells in autoimmune diseases with a focus on the emerging role of Bregs in regulating the balance between Tfh and Tfr cells. The previously unsuspected crosstalk between Bregs and Tfh/Tfr cells will be beneficial to understand the cellular mechanisms of autoantibody production and evoke a revolution in immunotherapy for autoimmune diseases.

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Increased CCR7loPD-1hiC

Cited by 6 publications

References 38 publications

CD4+ T Cells in Chronic Hepatitis B and T Cell-Directed Immunotherapy

CD4+ T Cells in Chronic Hepatitis B and T Cell-Directed Immunotherapy

Novel Molecular Therapeutics Targeting Signaling Pathway to Control Hepatitis B Viral Infection

Frontiers of Autoantibodies in Autoimmune Disorders: Crosstalk Between Tfh/Tfr and Regulatory B Cells

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