The role of apoptosis (programmed cell death) in haemopoiesis and the immune system

Allen, PD; Newland, Adrian C.; Bustin, Stephen A.

doi:10.1016/0268-960x(93)90025-y

Cited by 69 publications

(41 citation statements)

References 81 publications

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“…Death by apoptosis is the endpoint of a large number of biological and signalling events (Allen et al, 1993;McCabe & Orrenius, 1992). The actual intracellular events occurring during HIV infection that trigger apoptosis have yet to be uncovered.…”

Section: Discussionmentioning

confidence: 99%

Productive infection and subsequent interaction of CD4-gp120 at the cellular membrane is required for HIV-induced apoptosis of CD4+ T cells

Corbeil

Richman

1995

Journal of General Virology

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Section: Discussionmentioning

confidence: 99%

Productive infection and subsequent interaction of CD4-gp120 at the cellular membrane is required for HIV-induced apoptosis of CD4+ T cells

Corbeil

Richman

1995

Journal of General Virology

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“…Thus, cytokines regulate survival of hematopoietic cells through the activation of multiple signaling pathways. In contrast, the removal of cytokines rapidly inactivates these cell survival signals and results in massive apoptotic cell death (1,5).…”

mentioning

confidence: 99%

“…Hematopoietic cells require an appropriate cytokine(s) for their survival; in the absence of cytokines, these cells not only cease proliferation, but also undergo rapid apoptotic death (1). The strict dependence of hematopoietic cells on cytokines is the key to hematopoietic homeostasis.…”

mentioning

confidence: 99%

Requirement of the Caspase-3/CPP32 Protease Cascade for Apoptotic Death following Cytokine Deprivation in Hematopoietic Cells

Ohta¹,

Kinoshita²,

Naito³

et al. 1997

Journal of Biological Chemistry

101

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Hematopoietic cytokines transduce cell survival signals, which are distinct from the signals necessary for the stimulation of DNA synthesis. Recently, the Ras and phosphatidylinositol 3-kinase pathways have been shown to play important roles in preventing apoptosis in various cell types, e.g. hematopoietic cells and neuronal cells. Withdrawal of cytokine(s), in turn, results in rapid inactivation of these survival pathways and eventually leads to cell death accompanied by the hallmarks of apoptosis. However, the mechanism of cell death caused by cytokine deprivation has not been fully elucidated. In this study, we demonstrate that caspase-3/ CPP32, a member of the caspase/interleukin-1␤-converting enzyme family, is activated upon interleukin (IL)-3 deprivation in IL-3-dependent cells as well as IL-2 deprivation in IL-2-dependent cells. In addition, poly(ADPribose) polymerase, a cellular substrate for the caspase family proteases, was degraded into apoptotic fragments in both cell lines after cytokine removal. Furthermore, inhibition of a caspase family protease by synthetic peptides suppressed apoptotic death. These results indicate that the activation of a caspase-like protease(s) is required for the progression of apoptosis following cytokine deprivation. However, readdition of IL-3 did not restore the proliferative potential of the cells that survived in the presence of the peptide inhibitor after IL-3 depletion. Therefore, cellular commitment to apoptosis appears to precede the activation of a caspase-like protease(s).

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“…The term 'apoptosis' is reasonably equated with physiological cell death during immunological selection and biological development (Wyllie, 1987;Allen et al, 1993). It is also recognized that this mode of cell death is induced by certain markedly non-physiological stimuli exemplified by radiation and certain drugs and specifically including most agents used in cancer chemotherapy (Hickman, 1992;Sachs and Lotem, 1993;da Silva et al, 1996).…”

mentioning

confidence: 99%

Drug-induced death of leukaemic cells after G2/M arrest: higher order DNA fragmentation as an indicator of mechanism

Sleiman

Catchpoole²,

Stewart³

1998

Br J Cancer

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Summary Many reports have documented apoptotic death in different cell types within hours of exposure to cytotoxic drugs; lower drug concentrations may cause cell cycle arrest at G/M and subsequent death, which has been distinguished from 'classic' apoptosis. We have analysed etoposide-induced cell death in two lymphoblastoid T-cell lines, CCRF-CEM and MOLT-4, specifically in relation to DNA cleavage as indicated by pulse-field gel and conventional electrophoresis. High (5,M) concentration etoposide causes 50-kb cleavage of DNA that occurs at the same time as apoptotic morphology and internucleosomal cleavage. At lower concentrations (0.5-0.05 ,UM), sequential change may be discerned with altered gene expression being similar to that at high dose, but preceding cell cycle arrest and 50-kb cleavage. These last changes, in turn, clearly precede internucleosomal fragmentation of DNA, vital dye staining and morphological evidence cell death. The pattern of higher order fragmentation constitutes a sensitive indicator of commitment to cell death in these cells. Morphological evidence of cell death is associated with internucleosomal fragmentation in one of the lines, but the pattern of 50-kb DNA cleavage provides the clearest evidence of commonality in death processes occurring at low and high drug concentration.

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The role of apoptosis (programmed cell death) in haemopoiesis and the immune system

Cited by 69 publications

References 81 publications

Productive infection and subsequent interaction of CD4-gp120 at the cellular membrane is required for HIV-induced apoptosis of CD4+ T cells

Productive infection and subsequent interaction of CD4-gp120 at the cellular membrane is required for HIV-induced apoptosis of CD4+ T cells

Requirement of the Caspase-3/CPP32 Protease Cascade for Apoptotic Death following Cytokine Deprivation in Hematopoietic Cells

Drug-induced death of leukaemic cells after G2/M arrest: higher order DNA fragmentation as an indicator of mechanism

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