Human immunodeficiency virus (HIV-1) infection selectively downregulates PD-1 expression in infected cells and protects the cells from early apoptosis in vitro and in vivo.
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Summary
It is reported that productively infected CD4+ T cells lose PD-1, whereas bystander cells were unaffected, and p24+/PD-1 negative cells are less susceptible to apoptosis compared to bystanderser cells in the same infected milieu, suggesting a dual role for PD- 1 during HIV-1 infection.
- Type
- article
- Published
- 2008-06-20
- Cited by
- 24
- References
- 41
- Access
- Open access
- OpenAlex
- https://openalex.org/W2002789383
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:12045982
Keywords
Biology, Apoptosis, Bystander effect, In vivo, In vitro
References
- Distinct Mechanisms of CD4+ and CD8+ T-Cell Activation and Bystander Apoptosis Induced by Human Immunodeficiency Virus Type 1 Virions
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- Mechanisms of HIV‐1 to escape from the host immune surveillance
- The HIV-1 vpr Protein Acts as a Negative Regulator of Apoptosis in a Human Lymphoblastoid T Cell Line: Possible Implications for the Pathogenesis of AIDS
- Alternative splice variants of the human PD-1 gene.
- Dendritic Cells Infected with vpr-Positive Human Immunodeficiency Virus Type 1 Induce CD8+ T-Cell Apoptosis via Upregulation of Tumor Necrosis Factor Alpha
- Apoptosis occurs predominantly in bystander cells and not in productively infected cells of HIV- and SIV-infected lymph nodes
- PD-1 expression on HIV-specific T cells is associated with T-cell exhaustion and disease progression
- Rapid Expression of Human Immunodeficiency Virus following Activation of Latently Infected Cells
- A novel mechanism for HIV1-mediated bystander CD4+ T-cell death: neighboring dying cells drive the capacity of HIV1 to kill noncycling primary CD4+ T cells
- The downregulation of CD4 and MHC‐I by primate lentiviruses: a paradigm for the modulation of cell surface receptors
- Dynamics of cytokine expression in HIV productively infected primary CD4+ T cells.
- SIV-specific CD8+ T cells express high levels of PD1 and cytokines but have impaired proliferative capacity in acute and chronic SIVmac251 infection.
- PD-1 up-regulation is correlated with HIV-specific memory CD8+ T-cell exhaustion in typical progressors but not in long-term nonprogressors.
- Upregulation of PD-1 expression on HIV-specific CD8+ T cells leads to reversible immune dysfunction
- Retroviral infection of non-dividing cells: old and new perspectives.
- CD4+PD-1+ T cells acting as regulatory cells during the induction of anterior chamber-associated immune deviation.
Cited by
- The co-receptor signaling model of HIV-1 pathogenesis in peripheral CD4 T cells
- 'Omics investigations of HIV and SIV pathogenesis and innate immunity.
- TLR4 Activation Enhances the PD-L1-Mediated Tolerogenic Capacity of Colonic CD90+ Stromal Cells,
- CO-INHIBITORY MOLECULE PROGRAMMED DEATH-1 AND ITS LIGANDS: A NEW ALTERNATIVE THERAPY FOR HUMAN IMMUNODEFICIENCY VIRUS INFECTION?
- T-regulatory cells infected with feline immunodeficiency virus up-regulate programmed death-1 (PD-1).
- Comparative Expression Profile of miRNA and mRNA in Primary Peripheral Blood Mononuclear Cells Infected with Human Immunodeficiency Virus (HIV-1)
- Feline programmed death and its ligand: characterization and changes with feline immunodeficiency virus infection.
- MicroRNA regulation and its effects on cellular transcriptome in Human Immunodeficiency Virus-1 (HIV-1) infected individuals with distinct viral load and CD4 cell counts
- Programmed death (PD)‐1 molecule and its ligand PD‐L1 distribution among memory CD4 and CD8 T cell subsets in human immunodeficiency virus‐1‐infected individuals
- Drug-Induced Reactivation of Apoptosis Abrogates HIV-1 Infection
- Virus‐specific CD8 T cells: activation, differentiation and memory formation
- Chemokine Coreceptor Signaling in HIV-1 Infection and Pathogenesis
- Programmed death-1 expression is associated with the disease status in hepatitis B virus infection.
- Immune activation, apoptosis, and Treg activity are associated with persistently reduced CD4+ T-cell counts during antiretroviral therapy
- B and T lymphocyte attenuator down-regulation by HIV-1 depends on type I interferon and contributes to T-cell hyperactivation.
- The second chance story of HIV-1 DNA: Unintegrated? Not a problem!
- Delayed administration of anti‐PD‐1 antibody reverses immune dysfunction and improves survival during sepsis
- High T-cell immune activation and immune exhaustion among individuals with suboptimal CD4 recovery after 4 years of antiretroviral therapy in an African cohort
- HIV‐1 Infection Dysregulates Cell Cycle Regulatory Protein p21 in CD4+ T Cells Through miR‐20a and miR‐106b Regulation
- Germinal Center T Follicular Helper Cells (GC TFH) are Highly Permissive to HIV-1 and Alter Their Phenotype During Virus Replication
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