CD32
            <sup>+</sup>
            and PD-1
            <sup>+</sup>
            Lymph Node CD4 T Cells Support Persistent HIV-1 Transcription in Treated Aviremic Individuals

Noto, Alessandra; Procopio, Francesco A.; Banga, Riddhima; Suffiotti, Madeleine; Corpataux, Jean-Marc; Cavassini, Matthias; Riva, Agostino; Fenwick, Craig; Gottardo, Raphaël; Perreau, Matthieu; Pantaleo, Giuseppe

doi:10.1128/jvi.00901-18

Cited by 40 publications

(24 citation statements)

References 34 publications

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“…Subsequently, we compared the characteristics of CD4 + α4β7 + versus α4β7 - cells in terms of activation status (HLA-DR) and exhaustion status (PD-1) as well as CD39 and CCR5 expression ( Fig 3A–3D ). Cells that express high levels of the programmed cell death protein-1 (PD-1) have been shown to be a critical source of replication-competent HI virus in patients on ART [23,24]. Thus, the molecule has been proposed to be one of the markers describing the latent reservoir and its relation to α4β7 expression on different T-cell subsets is not known.…”

Section: Resultsmentioning

confidence: 99%

Comparison of the integrin α4β7 expression pattern of memory T cell subsets in HIV infection and ulcerative colitis

et al. 2019

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Anti-α4β7 therapy with vedolizumab (VDZ) has been suggested as possible immune intervention in HIV. Relatively little is known about the α4β7-integrin (α4β7) expression of different T-cell subsets in different anatomical compartments of healthy individuals, patients with HIV or inflammatory bowel disease (IBD). Surface expression of α4β7 as well as the frequency of activation, homing and exhaustion markers of T cells were assessed by multicolour flow cytometry in healthy volunteers (n = 15) compared to HIV infected patients (n = 52) or patients diagnosed with ulcerative colitis (UC) (n = 14), 6 of whom treated with vedolizumab. In addition, lymph nodal cells (n = 6), gut-derived cells of healthy volunteers (n = 5) and patients with UC (n = 6) were analysed. Additionally, we studied longitudinal PBMC samples of an HIV patient who was treated with vedolizumab for concomitant UC. Overall, only minor variations of the frequency of α4β7 on total CD4 + T cells were detectable regardless of the disease status or (VDZ) treatment status in peripheral blood and the studied tissues. Peripheral α4β7 + CD4 + T cells of healthy individuals and patients with UC showed a higher activation status and were more frequently CCR5 + than their α4β7 - counterparts. Also, the frequency of α4β7 + cells was significantly lower in peripheral blood CD4 + effector memory T cells of HIV-infected compared to healthy individuals and this reduced frequency did not recover in HIV patients on ART. Conversely, the frequency of peripheral blood naïve α4β7 + CD4 + T cells was significantly reduced under VDZ treatment. The results of the current study will contribute to the understanding of the dynamics of α4β7 expression pattern on T cells in HIV and UC and will be useful for future studies investigating VDZ as possible HIV cure strategy.

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Section: Resultsmentioning

confidence: 99%

Comparison of the integrin α4β7 expression pattern of memory T cell subsets in HIV infection and ulcerative colitis

et al. 2019

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“…Most activated CD4 + T-cells die from HIV cytopathogenicity or immune-mediated cell death. Compared with healthy controls, the expression levels of PD-1, CTLA-4, TIM-3, LAG-3, and TIGIT on effector CD4 + T-cells are elevated to varying degrees, accompanied by CD4 + T-cell function impairment and disease progression [47,[50][51][52][98][99][100]. For example, upregulation of PD-1 and CTLA-4 expression is associated with higher plasma viral loads and lower CD4 + T-cell counts.…”

Section: Hiv-specific T-cell Exhaustion Accompanies Immune Checkpointmentioning

confidence: 99%

Immune Checkpoints in Viral Infections

Cai

Liu

Zhong

et al. 2020

Viruses

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As evidence has mounted that virus-infected cells, such as cancer cells, negatively regulate the function of T-cells via immune checkpoints, it has become increasingly clear that viral infections similarly exploit immune checkpoints as an immune system escape mechanism. Although immune checkpoint therapy has been successfully used in cancer treatment, numerous studies have suggested that such therapy may also be highly relevant for treating viral infection, especially chronic viral infections. However, it has not yet been applied in this manner. Here, we reviewed recent findings regarding immune checkpoints in viral infections, including COVID-19, and discussed the role of immune checkpoints in different viral infections, as well as the potential for applying immune checkpoint blockades as antiviral therapy.

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“…Remarkably, we demonstrated a progressive increase in HIV DNA enrichment in CD32 + CD4 + cells with further purification of these cells, and in the purified population we measured a very prominent enrichment for HIV DNA (average, 292-fold) (106), confirming the results of Descours et al (99). Interestingly, several groups found that the majority of peripheral blood CD32 + CD4 + T cells express the activation marker HLA-DR (100–102, 106, 108, 109). Although it has been shown previously that HIV can establish latent infection in activated CD4 + T cells (110, 111) and that the peripheral blood HIV DNA load is higher in activated compared to resting cells in ART-treated individuals (112), the existence of latently infected CD4+ cells that are activated, and therefore relatively short-lived, suggests continuous replenishment of this component of the reservoir by cellular proliferation (113).…”

Section: Cd32amentioning

confidence: 99%

“…Two groups studied co-expression of CD32a and other HIV reservoir markers in tissues. Noto et al analyzed HIV transcription in LN memory CD4 + T-cell populations sorted for CD32a and PD-1 expression (108). The CD32 + and PD-1 + CD4 + T-cell populations overlapped to a large extent and CD32 + PD-1 + cells were significantly enriched for HIV RNA compared to CD32 − PD-1 − , CD32 + PD-1 − , and CD32 − PD-1 + cells.…”

Section: Cd32amentioning

confidence: 99%

The Quest for Cellular Markers of HIV Reservoirs: Any Color You Like

2019

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Combination antiretroviral therapy (ART) suppresses human immunodeficiency virus (HIV) replication and improves immune function, but is unable to eradicate the virus. Therefore, development of an HIV cure has become one of the main priorities of the HIV research field. The main obstacle for an HIV cure is the formation of latent viral reservoirs, where the virus is able to “hide” despite decades of therapy, just to reignite active replication once therapy is stopped. Revealing HIV hiding places is thus central to HIV cure research, but the absence of markers of these reservoir cells greatly complicates the search for a cure. Identification of one or several marker(s) of latently infected cells would represent a significant step forward toward a better description of the cell types involved and improved understanding of HIV latency. Moreover, it could provide a “handle” for selective therapeutic targeting of the reservoirs. A number of cellular markers of HIV reservoir have recently been proposed, including immune checkpoint molecules, CD2, and CD30. CD32a is perhaps the most promising of HIV reservoir markers as it is reported to be associated with a very prominent enrichment in HIV DNA, although this finding has been challenged. In this review, we provide an update on the current knowledge about HIV reservoir markers. We specifically highlight studies that characterized markers of persistently infected cells in the lymphoid tissues.

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CD32 ⁺ and PD-1 ⁺ Lymph Node CD4 T Cells Support Persistent HIV-1 Transcription in Treated Aviremic Individuals

Cited by 40 publications

References 34 publications

Comparison of the integrin α4β7 expression pattern of memory T cell subsets in HIV infection and ulcerative colitis

Comparison of the integrin α4β7 expression pattern of memory T cell subsets in HIV infection and ulcerative colitis

Immune Checkpoints in Viral Infections

The Quest for Cellular Markers of HIV Reservoirs: Any Color You Like

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CD32 + and PD-1 + Lymph Node CD4 T Cells Support Persistent HIV-1 Transcription in Treated Aviremic Individuals

Cited by 40 publications

References 34 publications

Comparison of the integrin α4β7 expression pattern of memory T cell subsets in HIV infection and ulcerative colitis

Comparison of the integrin α4β7 expression pattern of memory T cell subsets in HIV infection and ulcerative colitis

Immune Checkpoints in Viral Infections

The Quest for Cellular Markers of HIV Reservoirs: Any Color You Like

Contact Info

Product

Resources

About

CD32 ⁺ and PD-1 ⁺ Lymph Node CD4 T Cells Support Persistent HIV-1 Transcription in Treated Aviremic Individuals