Hepatitis C virus-induced NK cell activation causes metzincin-mediated CD16 cleavage and impaired antibody-dependent cytotoxicity

Oliviero, Barbara; Mantovani, Stefania; Varchetta, Stefania; Mele, Dalila; Grossi, Giulia; Ludovisi, Serena; Nuti, Elisa; Rossello, Armando; Mondelli, Mario U.

doi:10.1016/j.jhep.2017.01.032

Cited by 35 publications

(27 citation statements)

References 50 publications

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“…Third, and particularly worrisome, is the finding of incomplete reconstitution of MAIT cell frequencies in the liver and peripheral blood compartments after DAA treatment. A similar failure to restore immune function in chronic hepatitis C has been recently described for natural killer cell-mediated antibody-dependent cytotoxicity several weeks after sustained virologic response, 19 suggesting that HCV-induced alterations of selected innate immune responses may be long lasting or even permanent. The significance and implications of these findings remain to be elucidated.…”

supporting

confidence: 63%

Do Liver Mucosa-Associated Invariant T Cells Delay Hepatitis C Progression, or Are They Innocent Bystanders?

Mondelli

2017

Gastroenterology

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supporting

confidence: 63%

Do Liver Mucosa-Associated Invariant T Cells Delay Hepatitis C Progression, or Are They Innocent Bystanders?

Mondelli

2017

Gastroenterology

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“…In addition, the expression of FcγRIII, the CD16 activating receptor that is an essential mediator of ADCC, is downregulated on liver NK cells, which could explain the decrease in liver ADCC. CHCV infection induces NK cell activation, resulting in ADAM-17-dependent CD16 shedding and subsequent impairments in ADCC ( 43 ). Altered ADCC may contribute to the failure to eradicate the HCV infection.…”

Section: Discussionmentioning

confidence: 99%

“…According to a recent report ( 50 ), genetic factors largely determine the expression of inhibitory receptors, whereas activating receptors are substantially influenced by the environment. CHCV infection is known to induce NK cell activation ( 43 ). Therefore, the activation state of liver NK cells explains the restricted expression of KIR-activating genes in liver T cells, as well as the association of KIR-activating genes with CHCV infection.…”

Section: Discussionmentioning

confidence: 99%

The Clinical Features of Patients with Chronic Hepatitis C Virus Infections Are Associated with Killer Cell Immunoglobulin-Like Receptor Genes and Their Expression on the Surface of Natural Killer Cells

et al. 2018

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Killer cell immunoglobulin-like receptor (KIR) genes are known to play a role in the acute phase of hepatitis C virus (HCV) infection. The present study investigated their roles in chronic HCV (CHCV) infection by analyzing the phenotypes and function of natural killer (NK) and T cells that express KIRs. T cells from CHCV patients showed a more differentiated phenotype, and NK cells exhibited an activated profile. These observations are consistent with the increased expression of the degranulation marker CD107a observed after PMA stimulation. We explored the correlations between the expression of KIR genes and lectin type-C receptors with clinical factors that predict progression to fibrosis and cirrhosis. The expression levels of KIR2DS3 and the functional alleles of KIR2DS4-FL were increased in patients with intermediate and high viral loads. Homozygous KIR2DS4 was also associated with the presence of cirrhosis. In the group of individuals with a shorter infection time who developed cirrhosis, we detected decreased expression of KIR3DL1 in CD56dim NK cells in the presence of its ligand. Similarly, in the group of patients with late CHCV infections complicated with cirrhosis, we detected lower expression of the strong inhibitory receptor NKG2A in CD56bright NK cells. We also detected an increase in NKG2C expression in CD56dim NK cells in CHCV patients who displayed high necroinflammatory activity. Decreased KIR3DL2 expression in CD56dim and CD56bright NK cells was associated with a high body mass index, and KIR3DL2 expression may be one factor associated with the more rapid progression of CHCV to fibrosis in patients.

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“…Natural killer (NK) cells are essential innate immune cells which are able to directly kill unhealthy host cells, including virus-infected cells [1] and tumour cells [2]. Due to the downregulation of MHC I of virus-infected cells and tumour cells, the target cells can escape from the specific recognition of T cells [3].…”

Section: Introductionmentioning

confidence: 99%

The Roles of Siglec7 and Siglec9 on Natural Killer Cells in Virus Infection and Tumour Progression

Zheng

et al. 2020

Journal of Immunology Research

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The function of natural killer (NK) cells, defending against virus infection and tumour progression, is regulated by multiple activating and inhibiting receptors expressed on NK cells, among which sialic acid-bind immunoglobulin-like lectins (Siglecs) act as a vital inhibitory group. Previous studies have shown that Siglec7 and Siglec9 are expressed on NK cells, which negatively regulate the function of NK cells and modulate the immune response through the interaction of sialic acid-containing ligands. Siglec7 and Siglec9 are very similar in distribution, gene encoding, protein sequences, ligand affinity, and functions in regulating the immune system against virus and cancers, but differences still exist between them. In this review, we aim to discuss the similarities and differences between Siglec7 and Siglec9 and analyze their functions in virus infection and tumour progression in order to develop better anti-viral and anti-tumor immunotherapy in the future.

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Hepatitis C virus-induced NK cell activation causes metzincin-mediated CD16 cleavage and impaired antibody-dependent cytotoxicity

Cited by 35 publications

References 50 publications

Do Liver Mucosa-Associated Invariant T Cells Delay Hepatitis C Progression, or Are They Innocent Bystanders?

Do Liver Mucosa-Associated Invariant T Cells Delay Hepatitis C Progression, or Are They Innocent Bystanders?

The Clinical Features of Patients with Chronic Hepatitis C Virus Infections Are Associated with Killer Cell Immunoglobulin-Like Receptor Genes and Their Expression on the Surface of Natural Killer Cells

The Roles of Siglec7 and Siglec9 on Natural Killer Cells in Virus Infection and Tumour Progression

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