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  1. Article: CTL effector functions.

    Henkart, P A

    Seminars in immunology

    1997  Volume 9, Issue 2, Page(s) 85–86

    MeSH term(s) Animals ; Cell Degranulation ; Humans ; Immunity, Cellular ; T-Lymphocytes, Cytotoxic/enzymology ; T-Lymphocytes, Cytotoxic/immunology
    Language English
    Publishing date 1997-04
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1018141-6
    ISSN 1096-3618 ; 1044-5323
    ISSN (online) 1096-3618
    ISSN 1044-5323
    DOI 10.1006/smim.1997.0064
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: ICE family proteases: mediators of all apoptotic cell death?

    Henkart, P A

    Immunity

    1996  Volume 4, Issue 3, Page(s) 195–201

    MeSH term(s) Animals ; Apoptosis/immunology ; Caspase 1 ; Cell Death/immunology ; Cysteine Endopeptidases/immunology ; Humans ; Interleukin-1/immunology
    Chemical Substances Interleukin-1 ; Cysteine Endopeptidases (EC 3.4.22.-) ; Caspase 1 (EC 3.4.22.36)
    Language English
    Publishing date 1996-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/s1074-7613(00)80428-8
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  3. Article: Apoptosis: O death, where is thy sting?

    Henkart, P A

    Journal of immunology (Baltimore, Md. : 1950)

    1995  Volume 154, Issue 10, Page(s) 4905–4908

    MeSH term(s) Animals ; Apoptosis/genetics ; Apoptosis/physiology ; Cell Nucleus/physiology ; Humans ; Proto-Oncogene Proteins/physiology ; Proto-Oncogene Proteins c-bcl-2
    Chemical Substances Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2
    Language English
    Publishing date 1995-05-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
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  4. Article: Lymphocyte-mediated cytotoxicity: two pathways and multiple effector molecules.

    Henkart, P A

    Immunity

    1994  Volume 1, Issue 5, Page(s) 343–346

    MeSH term(s) Animals ; Cytotoxins/genetics ; Cytotoxins/pharmacology ; Gene Deletion ; Humans ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/pharmacology ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocytes, Cytotoxic/metabolism
    Chemical Substances Cytotoxins ; Membrane Glycoproteins ; Pore Forming Cytotoxic Proteins ; Perforin (126465-35-8)
    Language English
    Publishing date 1994-08
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/1074-7613(94)90063-9
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  5. Article: Mechanism of lymphocyte-mediated cytotoxicity.

    Henkart, P A

    Annual review of immunology

    1985  Volume 3, Page(s) 31–58

    MeSH term(s) Animals ; Antigens/immunology ; Cell Membrane/immunology ; Cytoplasmic Granules/immunology ; Cytotoxicity, Immunologic ; Exocytosis ; Humans ; In Vitro Techniques ; Killer Cells, Natural/immunology ; Lymphocytes/immunology ; Lymphocytes/secretion ; Lymphotoxin-alpha/immunology ; Mice ; Osmotic Pressure ; T-Lymphocytes, Cytotoxic/immunology
    Chemical Substances Antigens ; Lymphotoxin-alpha
    Language English
    Publishing date 1985
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604953-9
    ISSN 1545-3278 ; 0732-0582
    ISSN (online) 1545-3278
    ISSN 0732-0582
    DOI 10.1146/annurev.iy.03.040185.000335
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  6. Article: Apoptosis: mitochondria resurrected?

    Henkart, P A / Grinstein, S

    The Journal of experimental medicine

    1996  Volume 183, Issue 4, Page(s) 1293–1295

    MeSH term(s) Apoptosis/physiology ; Cell Nucleus/physiology ; Ion Channels/metabolism ; Mitochondria/physiology ; Signal Transduction
    Chemical Substances Ion Channels
    Language English
    Publishing date 1996-04-01
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.183.4.1293
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  7. Article: Role of reactive oxygen intermediates in TCR-induced death of T cell blasts and hybridomas.

    Williams, M S / Henkart, P A

    Journal of immunology (Baltimore, Md. : 1950)

    1996  Volume 157, Issue 6, Page(s) 2395–2402

    Abstract: The functional role of reactive oxygen intermediates (ROI) in activation-induced death of mature T lymphocytes and hybridomas was tested using antioxidants and inhibitors of enzymes that generate oxidants. These agents were shown to inhibit TCR-triggered ...

    Abstract The functional role of reactive oxygen intermediates (ROI) in activation-induced death of mature T lymphocytes and hybridomas was tested using antioxidants and inhibitors of enzymes that generate oxidants. These agents were shown to inhibit TCR-triggered death in a concentration-dependent manner, suggesting a possible role of ROI in this death. Since the TCR-induced death of both human T blasts and the murine T cell hybridoma 2B4 involve an initial step of TCR-induced Fas ligand (FasL) up-regulation followed by a lethal step induced by Fas cross-linking, both steps were examined separately for ROI dependence. The thiol antioxidants N-acetyl cysteine and glutathione blocked Fas-induced death triggered via cross-linking either by IgM anti-Fas or cell-bound FasL, while the other inhibitors of activation-induced death did not block this late lethal step. None of the agents used blocked early events after TCR ligation, as seen by the lack of inhibition of IL-2 secretion or CD69 up-regulation. However, the nonthiol agents that blocked activation-induced death all blocked FasL up-regulation induced by TCR signals in the hybridoma, as measured by a functional assay. Agents inhibiting FasL up-regulation also inhibited activation-induced ROI generation in the hybridoma, as detected by flow cytometry using dihydrorhodamine oxidation. Furthermore, a good correlation was found between the extent of ROI generation and functional FasL expression in 2B4 cells. Thus, while ROI do not appear to act as downstream mediators of apoptotic death induced by steroid or Fas cross-linking in T cells, they are generated by TCR signaling and appear to participate in FasL up-regulation.
    MeSH term(s) Animals ; Antioxidants/pharmacology ; Cell Death/drug effects ; Fas Ligand Protein ; Humans ; Hybridomas/drug effects ; Hybridomas/metabolism ; Ligands ; Lymphocyte Activation/drug effects ; Membrane Glycoproteins/biosynthesis ; Mice ; Oxygen/antagonists & inhibitors ; Reactive Oxygen Species/metabolism ; Reactive Oxygen Species/physiology ; Receptors, Antigen, T-Cell/drug effects ; Receptors, Antigen, T-Cell/physiology ; Sulfhydryl Compounds/pharmacology ; T-Lymphocytes/drug effects ; T-Lymphocytes/metabolism ; fas Receptor/drug effects
    Chemical Substances Antioxidants ; FASLG protein, human ; Fas Ligand Protein ; Fasl protein, mouse ; Ligands ; Membrane Glycoproteins ; Reactive Oxygen Species ; Receptors, Antigen, T-Cell ; Sulfhydryl Compounds ; fas Receptor ; Oxygen (S88TT14065)
    Language English
    Publishing date 1996-09-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
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  8. Article: Lymphocyte mediated cytolysis as a secretory phenomenon.

    Henkart, M P / Henkart, P A

    Advances in experimental medicine and biology

    1982  Volume 146, Page(s) 227–247

    MeSH term(s) Animals ; Antibody-Dependent Cell Cytotoxicity ; Antigens, Surface/immunology ; Cell Membrane/immunology ; Cytotoxicity, Immunologic ; Humans ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Kinetics ; Lymphocytes/immunology ; Lymphocytes/ultrastructure ; Microscopy, Electron
    Chemical Substances Antigens, Surface
    Language English
    Publishing date 1982
    Publishing country United States
    Document type Journal Article
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-1-4684-8959-0_13
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  9. Article: Cytotoxic lymphocytes. Two ways to kill target cells.

    Henkart, P A / Sitkovsky, M V

    Current biology : CB

    1994  Volume 4, Issue 10, Page(s) 923–925

    Abstract: Of the two pathways implicated in target-cell damage by cytotoxic lymphocytes, secretory granule exocytosis seems to dominate in anti-viral immunity whereas the Fas pathway may regulate immune responses. ...

    Abstract Of the two pathways implicated in target-cell damage by cytotoxic lymphocytes, secretory granule exocytosis seems to dominate in anti-viral immunity whereas the Fas pathway may regulate immune responses.
    MeSH term(s) Animals ; Antigens, Surface/physiology ; Cytoplasmic Granules/metabolism ; Cytotoxicity, Immunologic ; Exocytosis ; Humans ; T-Lymphocytes, Cytotoxic/immunology ; Virus Diseases/immunology ; fas Receptor
    Chemical Substances Antigens, Surface ; fas Receptor
    Language English
    Publishing date 1994-10-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 1071731-6
    ISSN 1879-0445 ; 0960-9822
    ISSN (online) 1879-0445
    ISSN 0960-9822
    DOI 10.1016/s0960-9822(00)00207-4
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  10. Article: Apoptotic cell death induced by intracellular proteolysis.

    Williams, M S / Henkart, P A

    Journal of immunology (Baltimore, Md. : 1950)

    1994  Volume 153, Issue 9, Page(s) 4247–4255

    Abstract: To mimic the injection of granzymes into target cells by cytotoxic lymphocytes or the activation of endogenous proteases in programmed cell death, the proteases chymotrypsin, proteinase K, or trypsin were loaded into the cytoplasm of several different ... ...

    Abstract To mimic the injection of granzymes into target cells by cytotoxic lymphocytes or the activation of endogenous proteases in programmed cell death, the proteases chymotrypsin, proteinase K, or trypsin were loaded into the cytoplasm of several different cell types using the osmotic lysis of pinosomes technique. Internalization of these proteases caused cell lysis within several hours, accompanied by extensive nuclear damage in most but not all combinations of target cells and proteases. This nuclear damage, quantitated by DNA release from nuclei, was associated with apoptotic features including DNA fragmentation into nucleosomal ladders, chromatin condensation, nuclear fragmentation, and membrane blebbing. Agents reported to block programmed cell death, including aurintricarboxylic acid, inhibitors of energy metabolism, and protein or RNA synthesis, failed to block this protease-induced death, although some inhibited nuclear damage. In separate experiments, introduction of staphylococcal nuclease into cells led to near complete (at least 75% of total) nucleosomal DNA fragmentation within 6 to 8 h. Condensation of chromatin did not accompany this fragmentation to the same extent, and there was approximately a 10-h lag between half-maximal DNA fragmentation and 50% loss of membrane integrity. The results suggest that activation of intracellular proteases during cell death by any molecular pathway could give rise to apoptotic morphology and DNA fragmentation.
    MeSH term(s) Apoptosis/physiology ; Cell Nucleus/metabolism ; Cell Nucleus/ultrastructure ; DNA/metabolism ; Endopeptidases/physiology ; Micrococcal Nuclease/metabolism ; Osmosis/physiology ; Tumor Cells, Cultured
    Chemical Substances DNA (9007-49-2) ; Micrococcal Nuclease (EC 3.1.31.1) ; Endopeptidases (EC 3.4.-)
    Language English
    Publishing date 1994-11-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
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