Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009

Kroemer, Guido; Galluzzi, Lorenzo; Vandenabeele, Peter; Abrams, John; Alnemri, Emad S.; Baehrecke, Eric H.; Blagosklonny, Mikhail V.; El‐Deiry, Wafik S.; Golstein, Pierre; Green, Douglas R.; Hengartner, Michael O.; Knight, Richard; Kumar, Sharad; Lipton, Stuart A.; Malorni, Walter; Núñez, Gabriel; Marynen, Peter; Tschopp, Jürg; Yuan, Junying; Piacentini, Mauro; Zhivotovsky, Boris; Melino, Gerry

doi:10.1038/cdd.2008.150

Cited by 2,511 publications

(1,459 citation statements)

References 92 publications

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“…39 In addition, p53-deficient cells responding to high-dose reversine manifested an early Δψ m dissipation, which is a widely accepted biochemical sign of the intrinsic pathway of apoptosis. 39,46 In line with this observation, the death of TP53 -/-HCT 116 cells as induced by high-dose reversine was exacerbated by the knockdown of anti-apoptotic Bcl-2-like proteins and inhibited by the depletion of pro-apoptotic Bcl-2 family members or APAF-1 as well as by the chemical inhibition of caspases.…”

Section: Methodssupporting

confidence: 54%

Preferential killing of p53-deficient cancer cells by reversine

et al. 2012

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Section: Methodssupporting

confidence: 54%

Preferential killing of p53-deficient cancer cells by reversine

et al. 2012

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“…1A). 24 We analyzed DNA fragmentation by means of a TUNEL assay and assessed ANXA5 binding. We could show stat.ph.…”

Section: Resultsmentioning

confidence: 99%

“…24 We performed cell cycle analysis, TUNEL staining, combined with a phosphatidylserine (PS) specific antibody as well as ANXA5 (annexin V) stainings on different growth stages of Lm promastigotes. By cell cycle analysis we could demonstrate that only a minority (20.8% § 1.1) of the Leishmania infectious inoculum, defined as stationary growth phase Lm (stat.ph.…”

Section: Resultsmentioning

confidence: 99%

Apoptotic-likeLeishmaniaexploit the host´s autophagy machinery to reduce T-cell-mediated parasite elimination

et al. 2015

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Apoptosis is a well-defined cellular process in which a cell dies, characterized by cell shrinkage and DNA fragmentation. In parasites like Leishmania, the process of apoptosis-like cell death has been described. Moreover upon infection, the apoptotic-like population is essential for disease development, in part by silencing host phagocytes. Nevertheless, the exact mechanism of how apoptosis in unicellular organisms may support infectivity remains unclear. Therefore we investigated the fate of apoptotic-like Leishmania parasites in human host macrophages. Our data showed-in contrast to viable parasites-that apoptotic-like parasites enter an LC3 C , autophagy-like compartment. The compartment was found to consist of a single lipid bilayer, typical for LC3-associated phagocytosis (LAP). As LAP can provoke anti-inflammatory responses and autophagy modulates antigen presentation, we analyzed how the presence of apoptotic-like parasites affected the adaptive immune response. Macrophages infected with viable Leishmania induced proliferation of CD4 C T-cells, leading to a reduced intracellular parasite survival. Remarkably, the presence of apoptotic-like parasites in the inoculum significantly reduced T-cell proliferation. Chemical induction of autophagy in human monocyte-derived macrophage (hMDM), infected with viable parasites only, had an even stronger proliferationreducing effect, indicating that host cell autophagy and not parasite viability limits the T-cell response and enhances parasite survival. Concluding, our data suggest that apoptotic-like Leishmania hijack the host cells´autophagy machinery to reduce T-cell proliferation. Furthermore, the overall population survival is guaranteed, explaining the benefit of apoptosis-like cell death in a single-celled parasite and defining the host autophagy pathway as a potential therapeutic target in treating Leishmaniasis.

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“…[1][2][3] In addition, MOMP is involved in some instances of apoptosis as elicited by extracellular signals of distress as well as in non-apoptotic forms of cell death, including regulated necrosis. 4,5 Irrespective of the initiating mechanism, MOMP results in: (1) the dissipation of the mitochondrial transmembrane potential (ΔΨ m ), in turn engendering a complete arrest of mitochondrial ATP synthesis and other ΔΨ m -dependent activities (e.g., protein import) and (2) the term "mitochondrial permeability transition" (Mpt) refers to an abrupt increase in the permeability of the inner mitochondrial membrane to low molecular weight solutes.…”

Section: Introductionmentioning

confidence: 99%

Role of the c subunit of the F_OATP synthase in mitochondrial permeability transition

et al. 2013

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Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009

Cited by 2,511 publications

References 92 publications

Preferential killing of p53-deficient cancer cells by reversine

Preferential killing of p53-deficient cancer cells by reversine

Apoptotic-likeLeishmaniaexploit the host´s autophagy machinery to reduce T-cell-mediated parasite elimination

Role of the c subunit of the F_OATP synthase in mitochondrial permeability transition

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Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009

Cited by 2,511 publications

References 92 publications

Preferential killing of p53-deficient cancer cells by reversine

Preferential killing of p53-deficient cancer cells by reversine

Apoptotic-likeLeishmaniaexploit the host´s autophagy machinery to reduce T-cell-mediated parasite elimination

Role of the c subunit of the FOATP synthase in mitochondrial permeability transition

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Role of the c subunit of the F_OATP synthase in mitochondrial permeability transition