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  1. Article ; Online: Recovery of natural killer cell cytotoxicity in a p.A91V perforin homozygous patient following severe haemophagocytic lymphohistiocytosis.

    Jang, Helena S / Flinsenberg, Thijs W H / Lacaze, Paul / Thia, Kevin Y T / Noori, Tahereh / Fernando, Suran L / Kerridge, Ian / Riaz, Moeen / McNeil, John J / Blombery, Piers A / Trapani, Joseph A / Voskoboinik, Ilia

    British journal of haematology

    2020  Volume 190, Issue 3, Page(s) 458–461

    MeSH term(s) Epstein-Barr Virus Infections/complications ; Ferritins/blood ; Fibrinogen/analysis ; Hepatitis/etiology ; Homozygote ; Humans ; Killer Cells, Natural/immunology ; Loss of Function Mutation ; Lymphohistiocytosis, Hemophagocytic/etiology ; Lymphohistiocytosis, Hemophagocytic/immunology ; Male ; Mutation, Missense ; Perforin/genetics ; Perforin/immunology ; Young Adult
    Chemical Substances PRF1 protein, human ; Perforin (126465-35-8) ; Fibrinogen (9001-32-5) ; Ferritins (9007-73-2)
    Language English
    Publishing date 2020-04-27
    Publishing country England
    Document type Case Reports ; Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 80077-6
    ISSN 1365-2141 ; 0007-1048
    ISSN (online) 1365-2141
    ISSN 0007-1048
    DOI 10.1111/bjh.16660
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: The granzyme B gene is highly polymorphic in wild mice but essentially invariant in common inbred laboratory strains.

    Thia, Kevin Y T / Trapani, Joseph A

    Tissue antigens

    2007  Volume 70, Issue 3, Page(s) 198–204

    Abstract: Granzyme B is a 247 amino acid pro-apoptotic protease secreted by effector lymphocytes for the purpose of killing virus-infected cells. While the capacity of granzyme B to potently induce caspase-dependent apoptosis has long been recognized, it has only ... ...

    Abstract Granzyme B is a 247 amino acid pro-apoptotic protease secreted by effector lymphocytes for the purpose of killing virus-infected cells. While the capacity of granzyme B to potently induce caspase-dependent apoptosis has long been recognized, it has only recently been found that human and mouse granzyme B activate overlapping but distinct apoptotic pathways. To investigate a possible evolutionary basis for this observation, we sequenced the exons and flanking intronic sequences of the mouse Gzmb gene from a variety of inbred laboratory strains and wild mice. The sequences of 12/13 inbred strains encoded identical proteins, the exception being DBA/2, whose sequence varied at two amino acids. By contrast with the laboratory strains, there was extensive polymorphism in the Gzmb gene of 54 wild mice and 28 wild-derived inbred mice examined, resulting in 2-18 amino acid differences in the predicted proteins, a discrepancy rate of up to 7.3%. Many of these amino acid variations were found in rat and/or human granzyme B. The granzyme B allotype of inbred laboratory strains could be identified in only one of three geographically dispersed clans of wild mice and was absent from all 28 wild-derived inbred strains. The Gzmb gene of Mus musculus castaneus, a close relative of laboratory mice, encoded six amino acid differences compared with the laboratory strains, all of which were also found in corresponding positions in the granzyme B molecules of wild mice. Unlike the protease, the extended granzyme B recognition and cleavage site in Bid, a key pro-apoptotic substrate, was invariant.
    MeSH term(s) Amino Acid Sequence ; Animals ; Genetic Variation ; Granzymes/genetics ; Mice ; Mice, Inbred A ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Inbred DBA ; Mice, Inbred NOD ; Mice, Inbred NZB ; Molecular Sequence Data ; Polymorphism, Single-Stranded Conformational
    Chemical Substances Granzymes (EC 3.4.21.-)
    Language English
    Publishing date 2007-09
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120440-3
    ISSN 1399-0039 ; 0001-2815
    ISSN (online) 1399-0039
    ISSN 0001-2815
    DOI 10.1111/j.1399-0039.2007.00872.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Differential effects of BTK inhibitors ibrutinib and zanubrutinib on NK-cell effector function in patients with mantle cell lymphoma.

    Flinsenberg, Thijs W H / Tromedjo, Charnelle C / Hu, Nan / Liu, Ye / Guo, Yin / Thia, Kevin Y T / Noori, Tahereh / Song, Xiaomin / Aw Yeang, Han X / Tantalo, Daniela G / Handunnetti, Sasanka / Seymour, John F / Roberts, Andrew W / Ritchie, David / Koldej, Rachel / Neeson, Paul J / Wang, Lai / Trapani, Joseph A / Tam, Constantine S /
    Voskoboinik, Ilia

    Haematologica

    2020  Volume 105, Issue 2, Page(s) e76–e79

    MeSH term(s) Adenine/analogs & derivatives ; Adult ; Humans ; Lymphoma, Mantle-Cell/drug therapy ; Piperidines ; Protein Kinase Inhibitors/therapeutic use ; Pyrazoles ; Pyrimidines/therapeutic use
    Chemical Substances Piperidines ; Protein Kinase Inhibitors ; Pyrazoles ; Pyrimidines ; ibrutinib (1X70OSD4VX) ; zanubrutinib (AG9MHG098Z) ; Adenine (JAC85A2161)
    Language English
    Publishing date 2020-01-31
    Publishing country Italy
    Document type Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2019.220590
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Human perforin mutations and susceptibility to multiple primary cancers.

    Trapani, Joseph A / Thia, Kevin Y T / Andrews, Miles / Davis, Ian D / Gedye, Craig / Parente, Philip / Svobodova, Suzanne / Chia, Jenny / Browne, Kylie / Campbell, Ian G / Phillips, Wayne A / Voskoboinik, Ilia / Cebon, Jonathan S

    Oncoimmunology

    2013  Volume 2, Issue 4, Page(s) e24185

    Abstract: Loss-of-function mutations in the gene coding for perforin ( ...

    Abstract Loss-of-function mutations in the gene coding for perforin (
    Language English
    Publishing date 2013-04-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2645309-5
    ISSN 2162-402X ; 2162-4011
    ISSN (online) 2162-402X
    ISSN 2162-4011
    DOI 10.4161/onci.24185
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  5. Article ; Online: A natural genetic variant of granzyme B confers lethality to a common viral infection.

    Andoniou, Christopher E / Sutton, Vivien R / Wikstrom, Matthew E / Fleming, Peter / Thia, Kevin Y T / Matthews, Antony Y / Kaiserman, Dion / Schuster, Iona S / Coudert, Jerome D / Eldi, Preethi / Chaudhri, Geeta / Karupiah, Gunasegaran / Bird, Phillip I / Trapani, Joseph A / Degli-Esposti, Mariapia A

    PLoS pathogens

    2014  Volume 10, Issue 12, Page(s) e1004526

    Abstract: Many immune response genes are highly polymorphic, consistent with the selective pressure imposed by pathogens over evolutionary time, and the need to balance infection control with the risk of auto-immunity. Epidemiological and genomic studies have ... ...

    Abstract Many immune response genes are highly polymorphic, consistent with the selective pressure imposed by pathogens over evolutionary time, and the need to balance infection control with the risk of auto-immunity. Epidemiological and genomic studies have identified many genetic variants that confer susceptibility or resistance to pathogenic micro-organisms. While extensive polymorphism has been reported for the granzyme B (GzmB) gene, its relevance to pathogen immunity is unexplored. Here, we describe the biochemical and cytotoxic functions of a common allele of GzmB (GzmBW) common in wild mouse. While retaining 'Asp-ase' activity, GzmBW has substrate preferences that differ considerably from GzmBP, which is common to all inbred strains. In vitro, GzmBW preferentially cleaves recombinant Bid, whereas GzmBP activates pro-caspases directly. Recombinant GzmBW and GzmBP induced equivalent apoptosis of uninfected targets cells when delivered with perforin in vitro. Nonetheless, mice homozygous for GzmBW were unable to control murine cytomegalovirus (MCMV) infection, and succumbed as a result of excessive liver damage. Although similar numbers of anti-viral CD8 T cells were generated in both mouse strains, GzmBW-expressing CD8 T cells isolated from infected mice were unable to kill MCMV-infected targets in vitro. Our results suggest that known virally-encoded inhibitors of the intrinsic (mitochondrial) apoptotic pathway account for the increased susceptibility of GzmBW mice to MCMV. We conclude that different natural variants of GzmB have a profound impact on the immune response to a common and authentic viral pathogen.
    MeSH term(s) Alleles ; Amino Acid Sequence ; Animals ; Apoptosis ; CD8-Positive T-Lymphocytes/pathology ; CD8-Positive T-Lymphocytes/virology ; Caspases/metabolism ; Disease Models, Animal ; Genetic Variation/genetics ; Granzymes/analysis ; Granzymes/deficiency ; Granzymes/genetics ; Herpesviridae Infections/immunology ; Herpesviridae Infections/mortality ; Herpesviridae Infections/pathology ; Immunity, Innate/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Muromegalovirus/immunology ; Virus Diseases/immunology ; Virus Diseases/mortality ; Virus Diseases/pathology
    Chemical Substances Granzymes (EC 3.4.21.-) ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2014-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1004526
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  6. Article: A clathrin/dynamin- and mannose-6-phosphate receptor-independent pathway for granzyme B-induced cell death.

    Trapani, Joseph A / Sutton, Vivien R / Thia, Kevin Y T / Li, Yu Qin / Froelich, Christopher J / Jans, David A / Sandrin, Mauro S / Browne, Kylie A

    The Journal of cell biology

    2003  Volume 160, Issue 2, Page(s) 223–233

    Abstract: The 280-kD cation-independent mannose-6-phosphate receptor (MPR) has been shown to play a role in endocytic uptake of granzyme B, since target cells overexpressing MPR have an increased sensitivity to granzyme B-mediated apoptosis. On this basis, it has ... ...

    Abstract The 280-kD cation-independent mannose-6-phosphate receptor (MPR) has been shown to play a role in endocytic uptake of granzyme B, since target cells overexpressing MPR have an increased sensitivity to granzyme B-mediated apoptosis. On this basis, it has been proposed that cells lacking MPR are poor targets for cytotoxic lymphocytes that mediate allograft rejection or tumor immune surveillance. In the present study, we report that the uptake of granzyme B into target cells is independent of MPR. We used HeLa cells overexpressing a dominant-negative mutated (K44A) form of dynamin and mouse fibroblasts overexpressing or lacking MPR to show that the MPR/clathrin/dynamin pathway is not required for granzyme B uptake. Consistent with this observation, cells lacking the MPR/clathrin pathway remained sensitive to granzyme B. Exposure of K44A-dynamin-overexpressing and wild-type HeLa cells to granzyme B with sublytic perforin resulted in similar apoptosis in the two cell populations, both in short and long term assays. Granzyme B uptake into MPR-overexpressing L cells was more rapid than into MPR-null L cells, but the receptor-deficient cells took up granzyme B through fluid phase micropinocytosis and remained sensitive to it. Contrary to previous findings, we also demonstrated that mouse tumor allografts that lack MPR expression were rejected as rapidly as tumors that overexpress MPR. Entry of granzyme B into target cells and its intracellular trafficking to induce target cell death in the presence of perforin are therefore not critically dependent on MPR or clathrin/dynamin-dependent endocytosis.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Apoptosis/immunology ; Cell Membrane/drug effects ; Cell Membrane/immunology ; Cell Membrane/metabolism ; Clathrin/drug effects ; Clathrin/genetics ; Clathrin/metabolism ; Dynamins/drug effects ; Dynamins/genetics ; Dynamins/metabolism ; Endocytosis/drug effects ; Endocytosis/immunology ; Female ; Graft Rejection/genetics ; Graft Rejection/immunology ; Granzymes ; HeLa Cells ; Humans ; Killer Cells, Natural/enzymology ; Killer Cells, Natural/immunology ; Male ; Membrane Glycoproteins/immunology ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation/genetics ; Neoplasms/immunology ; Neoplasms/metabolism ; Perforin ; Pore Forming Cytotoxic Proteins ; Receptor, IGF Type 2/deficiency ; Receptor, IGF Type 2/drug effects ; Receptor, IGF Type 2/genetics ; Serine Endopeptidases/deficiency ; Serine Endopeptidases/immunology ; Serine Endopeptidases/pharmacology ; T-Lymphocytes, Cytotoxic/enzymology ; T-Lymphocytes, Cytotoxic/immunology
    Chemical Substances Clathrin ; Membrane Glycoproteins ; Pore Forming Cytotoxic Proteins ; Receptor, IGF Type 2 ; Perforin (126465-35-8) ; GZMB protein, human (EC 3.4.21.-) ; Granzymes (EC 3.4.21.-) ; Gzmb protein, mouse (EC 3.4.21.-) ; Serine Endopeptidases (EC 3.4.21.-) ; Dynamins (EC 3.6.5.5)
    Language English
    Publishing date 2003-01-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.200210150
    Database MEDical Literature Analysis and Retrieval System OnLINE

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