ArticleeLife2021
Peripheral natural killer cells in chronic hepatitis B patients display multiple molecular features of T cell exhaustion.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Natural killer cells against viral infection: from basic biology to immunotherapy.Precision clinical medicine · 2026Review
- Persistent loss of intrahepatic IFN-γ in HBV is linked to selective impairment of liver-resident CXCR6+NK cells despite long-term NUC therapy.JHEP reports : innovation in hepatology · 2026Article
- Dissecting antibody-mediated natural killer cell effects reveals a cytotoxic CX3CR1+KLRC2-CD16hi subset linked to hepatitis B virus outcomes.Clinical and molecular hepatology · 2026Article
- Mapping Current Research Status and Emerging Frontiers of T-Cell Exhaustion: A Comprehensive Data-Mining-Based Study.Annals of surgical oncology · 2026Article
- Disrupting Viral Persistence: CRISPR/Cas9-Based Strategies for Hepatitis B and C Treatment, and Challenges.Journal of cellular and molecular medicine · 2026Review
- The interplay between hepatitis B virus and antitumor drugs in the treatment of hepatocellular carcinoma.Clinical and experimental medicine · 2025Review
- Chronic HBV infection impairs the glucose metabolism and effector function of NK cells via HBsAg/IL-15/mTOR axis.Cell death & disease · 2025Article
- Serological and virological characterization of hepatitis B surface antigen-positive patients with or without Helicobacter pylori co-infection at the university of Gondar comprehensive specialized hospital, Northwest Ethiopia.BMC infectious diseases · 2025Article
- Characterization of ex vivo expanded natural killer cells for cancer immunotherapy.Immunology and cell biology · 2025Article
- LAG3 Marks Activated but Hyporesponsive NK Cells.European journal of immunology · 2025Article
- Hepatitis B virus promotes liver cancer by modulating the immune response to environmental carcinogens.Nature communications · 2025Article
- Antiviral therapy for hepatitis B virus infection is beneficial for the prognosis hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Article
- An assembled molecular signaling map of interleukin-24: a resource to decipher its multifunctional immunoregulatory role in pathophysiological conditions.Frontiers in immunology · 2025Article
- Clinical and biochemical characterization of hepatitis B surface antigen-positive patients with or withoutFrontiers in immunology · 2025Article
- Dysfunctional natural killer cells can be reprogrammed to regain anti-tumor activity.The EMBO journal · 2024Article
- Overview of the immunological mechanisms in hepatitis B virus reactivation: Implications for disease progression and management strategies.World journal of gastroenterology · 2024Review
- Unraveling the dynamic mechanisms of natural killer cells in viral infections: insights and implications.Virology journal · 2024Review
- Peripheral NK cell phenotypic alteration and dysfunctional state post hepatitis B subviral particles stimulation in CHB patients: evading immune surveillance.Frontiers in immunology · 2024Article
- Differences in the intrahepatic expression of immune checkpoint molecules on T cells and natural killer cells in chronic HBV patients.Frontiers in immunology · 2024Article
- The novel mechanism facilitating chronic hepatitis B infection: immunometabolism and epigenetic modification reprogramming.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antiviral effectors such as natural killer (NK) cells have impaired functions in chronic hepatitis B (CHB) patients. The molecular mechanism responsible for this dysfunction remains poorly characterised. We show that decreased cytokine production capacity of peripheral NK cells from CHB patients was associated with reduced expression of NKp30 and CD16, and defective mTOR pathway activity. Transcriptome analysis of patients NK cells revealed an enrichment for transcripts expressed in exhausted T cells suggesting that NK cell dysfunction and T cell exhaustion employ common mechanisms. In particular, the transcription factor TOX and several of its targets were over-expressed in NK cells of CHB patients. This signature was predicted to be dependent on the calcium-associated transcription factor NFAT. Stimulation of the calcium-dependent pathway recapitulated features of NK cells from CHB patients. Thus, deregulated calcium signalling could be a central event in both T cell exhaustion and NK cell dysfunction occurring during chronic infections.
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