Immune Dysfunctions of CD56neg NK Cells Are Associated With HIV-1 Disease Progression

Cao, Wen-Jing; Zhang, Xiaochang; Wan, Lin-Yu; Li, Qingyu; Mu, Xiuying; Guo, Ailing; Zhou, Ming‐Ju; Shen, L; Zhang, Chao; Fan, Xing; Jiao, Yan‐Mei; Xu, Ruonan; Zhou, Chun‐Bao; Yuan, Jin‐Hong; Wang, Shengqi; Wang, Fusheng; Song, Jin‐Wen

doi:10.3389/fimmu.2021.811091

Cited by 15 publications

(19 citation statements)

References 44 publications

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“…In future studies, the expression of CD16, CD56, and NKG2D, as well as the transcriptional profile [FOXP3, HIF-1, and AhR (138-141)], should be included in the flow cytometry experiments or assessed, e.g. by use of single-cell transcriptional RNA expression analysis (142). NKG2D can activate gd T cells in an innate TCR-independent manner and is expressed by the vast majority of Vd2 T cells (29,43,143,144).…”

Section: Discussionmentioning

confidence: 99%

Inversed Ratio of CD39/CD73 Expression on γδ T Cells in HIV Versus Healthy Controls Correlates With Immune Activation and Disease Progression

et al. 2022

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Backgroundγδ T cells are unconventional T cells that have been demonstrated to be crucial for the pathogenesis and potentially for the cure of HIV-1 infection. The ectonucleotidase CD39 is part of the purinergic pathway that regulates immune responses by degradation of pro-inflammatory ATP in concert with CD73. Few studies on the expression of the ectoenzymes CD73 and CD39 on human γδ T cells in HIV have been performed to date.MethodsPBMC of n=86 HIV-1-infected patients were compared to PBMC of n=26 healthy individuals using 16-color flow cytometry determining the surface expression of CD39 and CD73 on Vδ1 and Vδ2 T cells in association with differentiation (CD45RA, CD28, CD27), activation and exhaustion (TIGIT, PD-1, CD38, and HLA-DR), and assessing the intracellular production of pro- and anti-inflammatory cytokines (IL-2, TGF-ß, TNF-α, Granzyme B, IL-10, IFN-γ) after in vitro stimulation with PMA/ionomycin.ResultsCD39 and CD73 expression on γδ T cells were inversed in HIV infection which correlated with HIV disease progression and immune activation. CD39, but not CD73 expression on γδ T cells of ART-treated patients returned to levels comparable with those of healthy individuals. Only a small subset (<1%) of γδ T cells co-expressed CD39 and CD73 in healthy or HIV-infected individuals. There were significantly more exhausted and terminally differentiated CD39+ Vδ1 T cells regardless of the disease status. Functionally, IL-10 was only detectable in CD39+ γδ T cells after in vitro stimulation in all groups studied. Viremic HIV-infected patients showed the highest levels of IL-10 production. The highest percentage of IL-10+ cells was found in the small CD39/CD73 co-expressing γδ T-cell population, both in healthy and HIV-infected individuals. Also, CD39+ Vδ2 T cells produced IL-10 more frequently than their CD39+ Vδ1 counterparts in all individuals regardless of the HIV status.ConclusionsOur results point towards a potential immunomodulatory role of CD39+ and CD73+ γδ T cells in the pathogenesis of chronic HIV infection that needs further investigation.

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Section: Discussionmentioning

confidence: 99%

Inversed Ratio of CD39/CD73 Expression on γδ T Cells in HIV Versus Healthy Controls Correlates With Immune Activation and Disease Progression

et al. 2022

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“…Besides, the expression of CD39 on NK cells affects HIV pathogenesis. In this regard, the frequencies of CD39 + CD56 bright NK cells, CD39 + CD56 neg NK cells, and CD38 + CD39 + NK cells were correlated positively to HIV-viral load and negatively to CD4 count [ 37 , 68 , 69 ].…”

Section: Cd39 Expression and Rna Virus Infectionsmentioning

confidence: 99%

The Role of Cluster of Differentiation 39 (CD39) and Purinergic Signaling Pathway in Viral Infections

et al. 2023

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CD39 is a marker of immune cells such as lymphocytes and monocytes. The CD39/CD73 pathway hydrolyzes ATP and adenosine, which has a potent immunosuppressive effect. CD39 regulates the function of a variety of immunologic cells through the purinergic signaling pathways. CD39+ T cells have been implicated in viral infections, including Human Immunodeficiency Virus (HIV), Cytomegalovirus (CMV), viral hepatitis, and Corona Virus Disease 2019 (COVID-19) infections. The expression of CD39 is an indicator of lymphocyte exhaustion, which develops during chronicity. During RNA viral infections, the CD39 marker can profile the populations of CD4+ T lymphocytes into two populations, T-effector lymphocytes, and T-regulatory lymphocytes, where CD39 is predominantly expressed on the T-regulatory cells. The level of CD39 in T lymphocytes can predict the disease progression, antiviral immune responses, and the response to antiviral drugs. Besides, the percentage of CD39 and CD73 in B lymphocytes and monocytes can affect the status of viral infections. In this review, we investigate the impact of CD39 and CD39-expressing cells on viral infections and how the frequency and percentage of CD39+ immunologic cells determine disease prognosis.

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“…The depletion of CD4+ T cells and senescence of CD8+ T cells are common in HIV carriers, which could contribute to the deficiency of EBV-specific T cell immune responses in EBV-driven lymphoma ( Piriou et al., 2005 ; Hernández et al., 2018 ). The EBV control was reported to be compromised in EBV-driven lymphoma which coinfected with HIV due to the deficient EBNA1-specific CD4+/CD8+ T cells ( Münz et al., 2000 ; Piriou et al., 2005 ; Mavilio et al., 2005 ), as well as the differentiation of NK cells to a CD56-negative NK cell without protective effects ( Mavilio et al., 2005 ; Cao et al., 2021 ) in HIV carriers. Besides, the induction of the apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like (APOBEC) family, which was clarified as a DNA-modifying enzyme in HIV coinfection, might be another trigger for EBV-driven lymphoma by somatic mutation accumulation ( Venkatesan et al., 2018 ).…”

Section: Implication Of Diverse Microbial Interacts With Ebv In Ebv-d...mentioning

confidence: 99%

How Does Epstein–Barr Virus Interact With Other Microbiomes in EBV-Driven Cancers?

Wen

Han

et al. 2022

Front. Cell. Infect. Microbiol.

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The commensal microbiome refers to a large spectrum of microorganisms which mainly consists of viruses and bacteria, as well as some other components such as protozoa and fungi. Epstein–Barr virus (EBV) is considered as a common component of the human commensal microbiome due to its spread worldwide in about 95% of the adult population. As the first oncogenic virus recognized in human, numerous studies have reported the involvement of other components of the commensal microbiome in the increasing incidence of EBV-driven cancers. Additionally, recent advances have also defined the involvement of host–microbiota interactions in the regulation of the host immune system in EBV-driven cancers as well as other circumstances. The regulation of the host immune system by the commensal microbiome coinfects with EBV could be the implications for how we understand the persistence and reactivation of EBV, as well as the progression of EBV-associated cancers, since majority of the EBV persist as asymptomatic carrier. In this review, we attempt to summarize the possible mechanisms for EBV latency, reactivation, and EBV-driven tumorigenesis, as well as casting light on the role of other components of the microbiome in EBV infection and reactivation. Besides, whether novel microbiome targeting strategies could be applied for curing of EBV-driven cancer is discussed as well.

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Immune Dysfunctions of CD56neg NK Cells Are Associated With HIV-1 Disease Progression

Cited by 15 publications

References 44 publications

Inversed Ratio of CD39/CD73 Expression on γδ T Cells in HIV Versus Healthy Controls Correlates With Immune Activation and Disease Progression

Inversed Ratio of CD39/CD73 Expression on γδ T Cells in HIV Versus Healthy Controls Correlates With Immune Activation and Disease Progression

The Role of Cluster of Differentiation 39 (CD39) and Purinergic Signaling Pathway in Viral Infections

How Does Epstein–Barr Virus Interact With Other Microbiomes in EBV-Driven Cancers?

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