Role of CD95-activated caspase-1 processing of IL-1β in TCR-mediated proliferation of HIV-infected CD4+ T cells

Petit, Frédéric; Corbeil, Jacques; Lelièvre, Jean‐Daniel; Parseval, Laure Moutouh–de; Pinon, Grégory; Green, Douglas R.; Ameisen, Jean Claude; Estaquier, Jérǒme

doi:10.1002/1521-4141(200112)31:12<3513::aid-immu3513>3.0.co;2-j

Cited by 29 publications

(25 citation statements)

References 40 publications

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“…[64][65][66][67] We recently demonstrated that the incubation of resting CD4 þ T cells from healthy donors, even in the presence of an inhibitor of the viral replication, was sufficient to prime CD4 þ T cells for apoptosis in response to CD95 ligation. 68,69 This priming did not require further T-cell activation, suggesting that interactions between the virus and T cells are sufficient. In this study, we found that susceptibility to CD95-induced apoptosis and viral load were higher in SIVmac251-infected macaques that were progressors than in those that were slow progressors, and in animals infected with SIVmac251 than in animals infected with Dnef.…”

Section: Discussionmentioning

confidence: 86%

Caspase-dependent and -independent T-cell death pathways in pathogenic simian immunodeficiency virus infection: relationship to disease progression

et al. 2003

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Studies of human immunodeficiency virus (HIV) and nonhuman primate models of pathogenic and nonpathogenic simian immunodeficiency virus (SIV) infections have suggested that enhanced ex vivo CD4 T-cell death is a feature of pathogenic infection in vivo. However, the relative contributions of the extrinsic and intrinsic pathways to programmed T-cell death in SIV infection have not been studied. We report here that the spontaneous death rate of CD4 þ T cells from pathogenic SIVmac251-infected rhesus macaques ex vivo is correlated with CD4 T-cell depletion and plasma viral load in vivo. CD4 þ T cells from SIVmac251-infected macaques showed upregulation of the death ligand (CD95L) and of the proapoptotic proteins Bim and Bak, but not of Bax. Both CD4 þ and CD8 þ T cells from SIVmac251-infected macaques underwent caspase-dependent death following CD95 ligation. The spontaneous death of CD4 þ and CD8 þ T cells was not prevented by a decoy CD95 receptor or by a broad-spectrum caspase inhibitor (zVADfmk), suggesting that this form of cell death is independent of CD95/CD95L interaction and caspase activation. IL-2 and IL-15 prevented the spontaneous death of CD4 þ and CD8 þ T cells, whereas IL-10 prevented only CD8 T-cell death and IL-7 had no effect on T-cell death. Our results indicate that caspasedependent and caspase-independent pathways are involved in the death of T cells in pathogenic SIVmac251-infected primates.

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Section: Discussionmentioning

confidence: 86%

Caspase-dependent and -independent T-cell death pathways in pathogenic simian immunodeficiency virus infection: relationship to disease progression

et al. 2003

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“…Second, because the sensitivity of cells to death also depends on the degree and duration of immune activation (activation-induced cell death), individual variations may be related to life history and prior infections. Third, individual variations in chemokine receptor expression may determine CD4 ϩ T cell death because the sensitivity of CD4 ϩ T cells to die in vitro depends on the levels and on the nature of the chemokine receptors expressed (34,36,62,63). Herein, we found that a strain of SIV that uses CCR5 and BOB/GPR15 molecules as coreceptors causes death of noncycling primary CD4 ϩ T cells, and that ligation of those coreceptors induced CD4 ϩ T cell death.…”

Section: Cd4mentioning

confidence: 82%

Death of CD4+ T Cells from Lymph Nodes during Primary SIVmac251 Infection Predicts the Rate of AIDS Progression

Viollet

Monceaux

Petit

et al. 2006

The Journal of Immunology

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Immunological and virological events that occur during the earliest stages of SIV infection are now considered to have a major impact on subsequent disease progression. In the present study, we demonstrate a clear correlation between progression to AIDS and the rate of in vitro CD4+ (but not CD8+) T cell death in lymph nodes. The dying CD4+ T cells were effector memory T cells, which are critical for the immune response to pathogens. However, there was no correlation between the rate of the viral replication within lymph nodes and the extent of Fas ligand-mediated death, despite the increased sensitivity of CD4+ T cells to death in response to recombinant human Fas ligand. CD4+ T cell death was caspase and apoptosis-inducing factor independent but was clearly associated with mitochondrion damage. Interestingly, higher expression levels of the active form of Bak, a proapoptotic molecule involved in mitochondrial membrane permeabilization, were observed in SIV-infected macaques progressing more rapidly to AIDS. Finally, we demonstrated that the strain of SIV we used requires CCR5 and BOB/GRP15 molecules as coreceptors and caused death of unstimulated noncycling primary CD4+ T cells. Altogether, these results demonstrate that CD4+ T cell death occurring early after SIV infection is a crucial determinant of progression to AIDS and that it is mediated by the intrinsic death pathway.

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“…A robust increase in CD95 expression has been observed previously in T cells from HIV-1-positive children as compared with healthy controls, as well as increased sensitivity to CD95-mediated cell death (29). Therefore, we measured CD95 expression on CD4 ϩ and CD8 ϩ T cells by triple FACS staining.…”

Section: Cd95 Expression Is Correlated To Disease Status and Agementioning

confidence: 87%

Correlates of Delayed Disease Progression in HIV-1-Infected Kenyan Children

Chakraborty

A-S.

Sutton

et al. 2005

The Journal of Immunology

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Without treatment most HIV-1-infected children in Africa die before their third birthday (>89%) and long-term nonprogressors are rare. The mechanisms underlying nonprogression in HIV-1-infected children are not well understood. In the present study, we examined potential correlates of delayed HIV disease progression in 51 HIV-1-infected African children. Children were assigned to progression subgroups based on clinical characterization. HIV-1-specific immune responses were studied using a combination of ELISPOT assays, tetramer staining, and FACS analysis to characterize the magnitude, specificity, and functional phenotype of HIV-1-specific CD8+ and CD4+ T cells. Host genetic factors were examined by genotyping with sequence-specific primers. HIV-1 nef gene sequences from infecting isolates from the children were examined for potential attenuating deletions. Thymic output was measured by T cell rearrangement excision circle assays. HIV-1-specific CD8+ T cell responses were detected in all progression groups. The most striking attribute of long-term survivor nonprogressors was the detection of HIV-1-specific CD4+ Th responses in this group at a magnitude substantially greater than previously observed in adult long-term nonprogressors. Although long-term survivor nonprogressors had a significantly higher percentage of CD45RA+CD4+ T cells, nonprogression was not associated with higher thymic output. No protective genotypes for known coreceptor polymorphisms or large sequence deletions in the nef gene associated with delayed disease progression were identified. In the absence of host genotypes and attenuating mutations in HIV-1 nef, long-term surviving children generated strong CD4+ T cell responses to HIV-1. As HIV-1-specific helper cells support anti-HIV-1 effector responses in active disease, their presence may be important in delaying disease progression.

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Role of CD95-activated caspase-1 processing of IL-1β in TCR-mediated proliferation of HIV-infected CD4+ T cells

Cited by 29 publications

References 40 publications

Caspase-dependent and -independent T-cell death pathways in pathogenic simian immunodeficiency virus infection: relationship to disease progression

Caspase-dependent and -independent T-cell death pathways in pathogenic simian immunodeficiency virus infection: relationship to disease progression

Death of CD4+ T Cells from Lymph Nodes during Primary SIVmac251 Infection Predicts the Rate of AIDS Progression

Correlates of Delayed Disease Progression in HIV-1-Infected Kenyan Children

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