The Fas/FasL System and T Cell Apoptosis in HIV-1-Infected Lymphoid Tissue during Highly Active Antiretroviral Therapy

Dyrhol‐Riise, Anne Ma; Stent, Gianna; Røsok, Bård I.; Voltersvik, Pål; Olofsson, Jan; Åsjö, Birgitta

doi:10.1006/clim.2001.5101

Cited by 28 publications

(17 citation statements)

References 58 publications

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“…However, we cannot exclude the possibility that mechanisms other than the TRAIL-TRAIL R1 pathway are also operative in the apoptosis of T cells in lymphoid tissue. The interaction of Fas and FasL, which are both overexpressed in tonsils from HIVinfected patients, 37 is certainly a candidate in this regard. Although absent on apoptotic T cells in our lymph node stainings, Herbeuval et al 38 found higher levels of TRAIL R2 mRNA in tonsils from HIV progressors than in those from HIV nonprogressors.…”

Section: Discussionmentioning

confidence: 99%

Plasmacytoid dendritic cells express TRAIL and induce CD4+ T-cell apoptosis in HIV-1 viremic patients

Stary

Klein

Kohlhofer

et al. 2009

Blood

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Section: Discussionmentioning

confidence: 99%

Plasmacytoid dendritic cells express TRAIL and induce CD4+ T-cell apoptosis in HIV-1 viremic patients

Stary

Klein

Kohlhofer

et al. 2009

Blood

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“…[6][7][8][9] A number of processes have been proposed to account for the depletion of CD4 T cells. [10][11][12][13][14][15] The majority of HIV-infected CD4 T cells are resting memory cells in a latent state of infection, probably expressing only minute amounts of viral proteins, making their actual contribution to CD4 T-cell depletion unknown. 10,16,17 The aim of this study was to delineate the role that CD8 T cells play in CD4 T-cell depletion during HIV infection.…”

Section: Introductionmentioning

confidence: 99%

Peripheral blood mononuclear cells of HIV‐infected patients contain CD8 T cells that form conjugates with and kill HIV‐infected autologous CD4 T cells

et al. 2015

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Summary Peripheral blood mononuclear cells (PBMC) of untreated, HIV‐infected patients contain HIV‐specific CD8 T cells as well as their corresponding targets, HIV‐infected CD4 T cells. To determine if CD4 T‐cell depletion in HIV‐infected patients may result from autologous CD8–CD4 T‐cell interaction, CD8 and CD4 T cells procured from PBMC of acute and chronic untreated HIV‐infected patients were sorted and co‐incubated. Formation of CD8‐CD4 T‐cell conjugates was observed by fluorescence microscopy. Apoptosis of CD4 T cells in conjugation was recorded by digitized images and was further observed and measured by FACS using Annexin staining. Perforin expression in the CD8 T cells was measured using intracellular monoclonal perforin antibody staining. HIV DNA in the conjugated CD4 T cells was detected by in situ PCR. We found that 6·1 ± 0·5% of CD4 T cells from acute HIV‐infected patients and 3·0 ± 0·5% from chronic HIV‐infected patients formed CD8–CD4 T‐cell conjugates. Annexin binding and cell morphology typical of apoptosis were observed in the conjugated CD4 T cells. The majority of CD8 T cells that had conjugated to CD4 T cells expressed perforin. The conjugated CD4 T cells exhibited nuclear HIV DNA. CD8 T cells and HIV‐infected CD4 T cells, both procured from the PBMC of untreated HIV‐infected patients, form conjugates. Apoptotic lytic activity has been observed in the conjugated CD4 T cells. We propose that CD4 T‐cell annihilation in HIV‐infected patients results, at least in part, from the interactions of perforin‐rich CD8 T cells with autologous, HIV‐infected CD4 T cells.

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“…The contribution of the Fas/FasL system to CD4 T cell apoptosis during HIV-1 infection is well documented [149–151], and similar findings were reported for IFN-I-induced TRAIL and its death receptor (DR)5 [55, 65, 121, 152, 153]. TRAIL expression following HIV-1 exposure or infection has been described in T cells, monocytes, and pDC [24, 55, 153, 154], and TRAIL expressing pDC have been shown to directly induce apoptosis of CD4 T cells in HIV-1 infected patients with high viraemia [153].…”

Section: Effect Of Ifn-i On Target Cellsmentioning

confidence: 99%

Type I Interferon at the Interface of Antiviral Immunity and Immune Regulation: The Curious Case of HIV-1

Boasso

2013

Scientifica

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Type I interferon (IFN-I) play a critical role in the innate immune response against viral infections. They actively participate in antiviral immunity by inducing molecular mechanisms of viral restriction and by limiting the spread of the infection, but they also orchestrate the initial phases of the adaptive immune response and influence the quality of T cell immunity. During infection with the human immunodeficiency virus type 1 (HIV-1), the production of and response to IFN-I may be severely altered by the lymphotropic nature of the virus. In this review I consider the different aspects of virus sensing, IFN-I production, signalling, and effects on target cells, with a particular focus on the alterations observed following HIV-1 infection.

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The Fas/FasL System and T Cell Apoptosis in HIV-1-Infected Lymphoid Tissue during Highly Active Antiretroviral Therapy

Cited by 28 publications

References 58 publications

Plasmacytoid dendritic cells express TRAIL and induce CD4+ T-cell apoptosis in HIV-1 viremic patients

Plasmacytoid dendritic cells express TRAIL and induce CD4+ T-cell apoptosis in HIV-1 viremic patients

Peripheral blood mononuclear cells of HIV‐infected patients contain CD8 T cells that form conjugates with and kill HIV‐infected autologous CD4 T cells

Type I Interferon at the Interface of Antiviral Immunity and Immune Regulation: The Curious Case of HIV-1

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