Gotowe bibliografie tematyczne / Granzymes

Gotowa bibliografia na temat „Granzymes”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 maja 2022

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Artykuły w czasopismach na temat "Granzymes"

1

Joeckel, Lars T., i Phillip I. Bird. "Are all granzymes cytotoxic in vivo?" Biological Chemistry 395, nr 2 (1.02.2014): 181–202. http://dx.doi.org/10.1515/hsz-2013-0238.

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Abstract Granzymes are serine proteases mainly found in cytotoxic lymphocytes. The most-studied member of this group is granzyme B, which is a potent cytotoxin that has set the paradigm that all granzymes are cyototoxic. In the last 5 years, this paradigm has become controversial. On one hand, there is a plethora of sometimes contradictory publications showing mainly caspase-independent cytotoxic effects of granzyme A and the so-called orphan granzymes in vitro. On the other hand, there are increasing numbers of reports of granzymes failing to induce cell death in vitro unless very high (potentially supra-physiological) concentrations are used. Furthermore, experiments with granzyme A or granzyme M knock-out mice reveal little or no deficit in their cytotoxic lymphocytes’ killing ability ex vivo, but indicate impairment in the inflammatory response. These findings of non-cytotoxic effects of granzymes challenge dogma, and thus require alternative or additional explanations to be developed of the role of granzymes in defeating pathogens. Here we review evidence for granzyme cytotoxicity, give an overview of their non-cytotoxic functions, and suggest technical improvements for future investigations.
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2

Ebnet, K., C. N. Levelt, T. T. Tran, K. Eichmann i M. M. Simon. "Transcription of granzyme A and B genes is differentially regulated during lymphoid ontogeny." Journal of Experimental Medicine 181, nr 2 (1.02.1995): 755–63. http://dx.doi.org/10.1084/jem.181.2.755.

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During development, thymocytes express a number of genes typical for activated peripheral T lymphocytes, including granzymes. We have now analyzed by reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, and cytochemistry fetal liver cells and thymocytes at various developmental stages for the expression of granzyme A-G genes. At days 13-17 of gestation, only granzyme B but none of the other granzymes is expressed in fetal liver. In the most immature, Pgp-1+IL2R alpha-, thymocyte subpopulation mRNAs for granzymes A-C but not for granzymes D-G are detectable. Upon further differentiation via Pgp-1-IL-2R alpha + into more mature Pgp-1-IL-2R alpha- thymocytes the level of expression of granzymes A, B, and C gradually declines reaching its lowest level at the CD4+ 8+ double positive stage. In fetal thymic lobes depleted of lymphoid cells by treatment with deoxyguanosine, no transcripts for granzymes A, B, and C were found indicating that the PCR signals are derived exclusively from early precursor T/natural killer (NK) lineage cells rather than from residual stromal elements. In mature CD4+CD8- and CD4-CD8+ thymocytes, granzyme B mRNA is found at similar levels in both subsets whereas granzyme A mRNA is expressed selectively in the CD4-CD8+ subset. Enzymatic activity of granzyme A was only seen in a fraction of CD4-CD8+ thymocytes negative for heat stable antigen (HSA) but not in the more immature HSA+ fraction of CD4-CD8+ thymocytes. The data suggest that (a) granzyme B is a pro-thymocyte marker for all T/NK lineage cells; (b) granzyme A transcripts are associated with thymocytes with the potential to develop into the CD8+ lineage; and (c) granzyme A enzymatic activity is only expressed in the most mature CD4-CD8+ stage, suggesting that granzyme proteins are not involved in early stages of thymocyte development.
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3

Hay, Zachary L. Z., i Jill E. Slansky. "Granzymes: The Molecular Executors of Immune-Mediated Cytotoxicity". International Journal of Molecular Sciences 23, nr 3 (6.02.2022): 1833. http://dx.doi.org/10.3390/ijms23031833.

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Cytotoxic T lymphocytes, differentiated CD8+ T cells, use multiple mechanisms to mediate their function, including release of granules containing perforin and granzymes at target cells. Granzymes are a family of cytotoxic proteases that each act on unique sets of biological substrates within target cells, usually to induce cell death. Granzymes are differentially expressed within T cells, depending on their environment and activation state, making the granzyme cytotoxic pathway dynamic and responsive to individual circumstances. In this review, we describe what is currently known about granzyme structure, processing, and granzyme-induced cell death in the context of cancer and in some other inflammatory diseases.
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Grossman, William J., James W. Verbsky, Benjamin L. Tollefsen, Claudia Kemper, John P. Atkinson i Timothy J. Ley. "Differential expression of granzymes A and B in human cytotoxic lymphocyte subsets and T regulatory cells". Blood 104, nr 9 (1.11.2004): 2840–48. http://dx.doi.org/10.1182/blood-2004-03-0859.

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Abstract Cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells use the perforin/granzyme pathway as a major mechanism to kill pathogen-containing cells and tumor cells.1,2 Dysregulation of this pathway results in several human diseases, such as hemophagocytic lymphohistiocytosis. Here we characterize the single-cell expression pattern of granzymes A and B in human lymphocytes using a flow cytometry-based assay. We demonstrate that most circulating CD56+8- NK cells, and approximately half of circulating CD8+ T lymphocytes, coexpressed both granzymes A and B. In contrast, few circulating CD4+ T lymphocytes expressed granzymes A or B. Activation of CD8+ T lymphocytes with concanavalin A (ConA)/interleukin-2 (IL-2), and activation of CD4+ T lymphocytes with antibodies to CD3/CD28 or CD3/CD46 (to generate T regulatory [Tr1] cells), induced substantial expression of granzyme B, but not granzyme A. Naive CD4+CD45RA+ cells stimulated with antibodies to CD3/CD46 strongly expressed granzyme B, while CD3/CD28 stimulation was ineffective. Finally, we show that granzyme B-expressing CD4+ Tr1 cells are capable of killing target cells in a perforin-dependent, but major histocompatibility complex (MHC)/T-cell receptor (TCR)-independent, manner. Our results demonstrate discordant expression of granzymes A and B in human lymphocyte subsets and T regulatory cells, which suggests that different granzymes may play unique roles in immune system responses and regulation.
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5

Zeberg, Lennart, i Tor Olofsson. "Differential Expression of Granzymes A and K in Subsets of Human T-Cells and NK-Cells." Blood 106, nr 11 (16.11.2005): 3917. http://dx.doi.org/10.1182/blood.v106.11.3917.3917.

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Abstract Granzymes are highly specific proteases stored in secretory granule in T-cells and NK-cells. Five different granzymes are known in human (A, B, H, K and M). A and B are the best studied and both can induce apotosis when delivered to target cells. The role for granzyme H, K and M are principally unknown. We have studied the expression of granzymes in subsets of T-cells and NK-cells both in fresh circulating cells and cultured cells stimulated with IL-2, IL-15 and OKT3/antiCD28. Protein expression (biosynthesis/immunoprecipitation) and mRNA level (RT-PCR) was studied in parallel. This report focus on Granzyme A and K which are close relatives, both tryptases located 70 kb apart on chromosome 5. Granzyme A have the highest expression in NK-cells were granzyme K are barely detected. Granzyme K on the other hand have a particular high expression in CD8+ T cells. Stimulation with IL-2 or IL-15 give a strong upregulation of both enzymes in NK-cells. Stimulation of CD8+ T cells gives mainly upregulation of granzyme A. Fresh CD4+ T cells show very weak synthesis of granzymes but treatment with IL-2 or IL-15 give a clear upregulation of both granzyme A and K. T-cells (both CD4+ and CD8+) are highly responsive to stimulation with OKT3/anti CD28 producing granzyme B but not A and K. This rather discordant pattern of expression for granzyme A and K talks in favour of different modes of regulation and most likely different functions. A striking difference between granzyme A and K concern the propensity for granzyme A to be secreted into the culture medium after stimulation while this is not the case for granzyme K. The secreted form of granzyme A has a molecular weight slightly higher than the intracellular form indicating the presence of a proform. Secretion of granzymes to the extracellular medium is probably not only an in vitro phenomena since both granzyme A and B can be detected in serum from healthy individuals in picomolar concentrations. Moreover, significant elevation of granzyme levels in serum can bee seen in different diseases with activation of cellular immunity and in T- and NK-cells malignancies. We have previously reported that proforms of certain serine proteases including the five human granzymes have a downregulating activity on myeloid proliferation, a mechanism probably implicated in certain forms of neutropenia. We propose that secreted granzymes (especially A, B and H) constitute a part of T regulatory function working both locally at the site of inflammation and distantly via the circulation.
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6

Cao, Xuefang, Paula A. Revell, William J. Grossman, Dori A. Thomas, Zhi Hong Lu i Timothy J. Ley. "Orphan Granzymes Downstream from Granzyme B Are Important for Tumor Clearance In Vivo and in Vitro." Blood 104, nr 11 (16.11.2004): 2653. http://dx.doi.org/10.1182/blood.v104.11.2653.2653.

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Abstract Cytotoxic lymphocytes (Natural Killer cells and Cytotoxic T lymphocytes) can utilize the perforin/granzyme pathway as a major mechanism to kill pathogen-infected cells and tumor cells. Perforin is responsible for delivering and/or trafficking the granzymes (a family of neutral serine proteases) to the target cells. In the target cell cytoplasm and nucleus, the granzymes deliver the lethal hits. Granzymes A and B are the best characterized granzymes, and they can cleave a variety of important protein substrates to execute the target cells. However, some tumors and viruses have developed potent granzyme inhibitors that may allow them to evade cytotoxic lymphocyte-induced death. Interestingly, additional granzyme genes downstream from granzyme B (C, F, G, and D) on murine chromosome 14 are also expressed in cytotoxic lymphocytes, and are referred to as “orphans” since their functions have not been defined. We have developed two kinds of granzyme B knockout mice in the 129/SvJ background (H-2b) and examined their expression of granzyme B and orphan granzymes using quantitative RT-PCR and Western Blotting. In the first mouse (Gzm B−/−/+PGK-neo) a PGK-neo cassette was retained in the granzyme B gene, which caused a neighborhood effect, with significantly reduced expression of orphan granzymes C and F in cytotoxic lymphocytes (this mouse is referred to as “B cluster” deficient); In the second mouse (Gzm B−/−/ΔPGK-neo) the PGK-neo cassette was removed by Cre/loxP technology, which restored expression of granzymes C and F in cytotoxic lymphocytes (referred to as “B only” deficient). Both mutations completely abolish granzyme B expression. Using a Flow-based Killing Assay (FloKA), we have examined the cytotoxic functions of lymphocytes derived from mixed lymphocyte reactions (MLR) and 10-day lymphokine activated killer (LAK) cultures. We have found that granzyme B cluster-deficient cytotoxic lymphocytes (H-2b) generated by MLR kill allogeneic P815 or TA-3 tumor cells (H-2d) less efficiently than those deficient for granzyme B only (e.g. P815 killing at 3 hours, WT: 35%±1%, B only-deficient: 24%±5%, B cluster-deficient: 14%±3%, p<0.001). The reduction in granzyme B cluster-deficient killing is also seen with LAK cells against YAC-1 and RMA-S target cells (e.g. RMA-S killing at 4 hours, WT: 26%±1%, B only-deficient: 24%±1%, B cluster-deficient: 18%±1%, p<0.001). These results suggest that both allogeneic CTL and LAK cells require orphan granzymes (C and/or F) for optimal tumor cell killing. The defects in cytotoxicity detected by the FloKA assay have been confirmed to be biologically relevant (Revell et al, Blood2003, 102 (11): 1022) since granzyme B cluster-deficient mice cleared P815 cells less efficiently than either WT or granzyme B only-deficient mice (p<0.02). These studies suggest that the orphan granzymes are important for cytotoxic lymphocyte functions, and that they may provide a source of functional redundancy that would help protect from pathogens or tumor cells that express inhibitors of granzyme A or B.
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7

Kaiserman, Dion, Catherina H. Bird, Jiuru Sun, Antony Matthews, Kheng Ung, James C. Whisstock, Philip E. Thompson, Joseph A. Trapani i Phillip I. Bird. "The major human and mouse granzymes are structurally and functionally divergent". Journal of Cell Biology 175, nr 4 (20.11.2006): 619–30. http://dx.doi.org/10.1083/jcb.200606073.

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Approximately 2% of mammalian genes encode proteases. Comparative genomics reveals that those involved in immunity and reproduction show the most interspecies diversity and evidence of positive selection during evolution. This is particularly true of granzymes, the cytotoxic proteases of natural killer cells and CD8+ T cells. There are 5 granzyme genes in humans and 10 in mice, and it is suggested that granzymes evolve to meet species-specific immune challenge through gene duplication and more subtle alterations to substrate specificity. We show that mouse and human granzyme B have distinct structural and functional characteristics. Specifically, mouse granzyme B is 30 times less cytotoxic than human granzyme B and does not require Bid for killing but regains cytotoxicity on engineering of its active site cleft. We also show that mouse granzyme A is considerably more cytotoxic than human granzyme A. These results demonstrate that even “orthologous” granzymes have species-specific functions, having evolved in distinct environments that pose different challenges.
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Thiery, Jerome, Dennis Keefe, Saviz Saffarian, Denis Martinvalet, Michael Walch, Emmanuel Boucrot, Tomas Kirchhausen i Judy Lieberman. "Perforin activates clathrin- and dynamin-dependent endocytosis, which is required for plasma membrane repair and delivery of granzyme B for granzyme-mediated apoptosis". Blood 115, nr 8 (25.02.2010): 1582–93. http://dx.doi.org/10.1182/blood-2009-10-246116.

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Abstract Cytotoxic T lymphocytes and natural killer cells destroy target cells via the polarized exocytosis of lytic effector proteins, perforin and granzymes, into the immunologic synapse. How these molecules enter target cells is not fully understood. It is debated whether granzymes enter via perforin pores formed at the plasma membrane or whether perforin and granzymes are first endocytosed and granzymes are then released from endosomes into the cytoplasm. We previously showed that perforin disruption of the plasma membrane induces a transient Ca2+ flux into the target cell that triggers a wounded membrane repair response in which lysosomes and endosomes donate their membranes to reseal the damaged membrane. Here we show that perforin activates clathrin- and dynamin-dependent endocytosis, which removes perforin and granzymes from the plasma membrane to early endosomes, preserving outer membrane integrity. Inhibiting clathrin- or dynamin-dependent endocytosis shifts death by perforin and granzyme B from apoptosis to necrosis. Thus by activating endocytosis to preserve membrane integrity, perforin facilitates granzyme uptake and avoids the proinflammatory necrotic death of a membrane-damaged cell.
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9

Nakajima, H., H. L. Park i P. A. Henkart. "Synergistic roles of granzymes A and B in mediating target cell death by rat basophilic leukemia mast cell tumors also expressing cytolysin/perforin." Journal of Experimental Medicine 181, nr 3 (1.03.1995): 1037–46. http://dx.doi.org/10.1084/jem.181.3.1037.

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We have studied the cytotoxic activity of rat basophilic leukemia (RBL) cells transfected with cDNAs for the cytotoxic T lymphocyte (CTL) granule components, cytolysin (perforin), granzyme A, and granzyme B. With red cell targets, cytolysin expression conferred potent hemolytic activity, which was not influenced by coexpression of granzymes. With tumor targets, RBL cells expressing cytolysin alone were weakly cytotoxic, but both cytolytic and nucleolytic activity were enhanced by coexpression of granzyme B. RBL cells expressing all three CTL granule components showed still higher cytotoxic activities, with apoptotic target death. Analysis of the cytotoxic activity of individual transfectant clones showed that cytolytic and nucleolytic activity correlated with granzyme expression but was independent of cytolysin expression within the range examined. A synergism between granzymes A and B was apparent when the triple transfectant was compared with RBL cells expressing cytolysin and one granzyme. These data implicate granzymes as the major mediators of tumor target damage by cytotoxic lymphocytes.
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Griffiths, G. M., i S. Isaaz. "Granzymes A and B are targeted to the lytic granules of lymphocytes by the mannose-6-phosphate receptor." Journal of Cell Biology 120, nr 4 (15.02.1993): 885–96. http://dx.doi.org/10.1083/jcb.120.4.885.

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To investigate the question of whether lytic granules share a common biogenesis with lysosomes, cloned cytolytic T cell lines were derived from a patient with I-cell disease. The targeting of two soluble lytic granule components, granzymes A and B, was studied in these cells which lack a functional mannose-6-phosphate (Man-6-P) receptor-mediated pathway to lysosomes. Using antibodies and enzymatic substrates to detect the lytic proteins, I-cells were found to constitutively secrete granzymes A and B in contrast to normal cells in which these proteins were stored for regulated secretion. These results suggest that granzymes A and B are normally targeted to the lytic granules of activated lymphocytes by the Man-6-P receptor. In normal cells, the granzymes bear Man-6-P residues, since the oligosaccharide side chains of granzymes A and B, as well as radioactive phosphate on granzyme A from labeled cells, were removed by endoglycosidase H (Endo H). However, in I-cells, granzymes cannot bear Man-6-P and granzyme B acquires complex glycans, becoming Endo H resistant. Although the levels of granzymes A and B in cytolytic I-cell lymphocytes are < 30% of the normal levels, immunolocalization and cell fractionation of granzyme A demonstrated that this reduced amount is correctly localized in the lytic granules. Therefore, a Man-6-P receptor-independent pathway to the lytic granules must also exist. Cathepsin B colocalizes with granzyme A in both normal and I-cells indicating that lysosomal proteins can also use the Man-6-P receptor-independent pathway in these cells. The complete overlap of these lysosomal and lytic markers implies that the lytic granules perform both lysosomal and secretory roles in cytolytic lymphocytes. The secretory role of lytic granules formed by the Man-6-P receptor-independent pathway is intact as assessed by the ability of I-cell lymphocytes to lyse target cells by regulated secretion.
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Rozprawy doktorskie na temat "Granzymes"

1

Yang, Jie. "Characterization of bovine granzymes and studies of the role of granzyme B in killing of Theileria-infected cells by CD8+ T cells". Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6487.

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Previous studies have shown that cytotoxic CD8+ T cells are important mediators of immunity against the bovine intracellular protozoan parasite T. parva. The present study set out to determine the role of granule enzymes in mediating killing of parasitized cells, first by characterising the granzymes expressed by bovine lymphocytes and, second, by investigating their involvement in killing of target cells. Experiments using the perforin inhibitor concanamycin A confirmed that CD8+ T cell killing of T. parva-infected cells is dependent on granule exocytosis, a process that involves release of granzymes into the target cell, resulting in activation of apoptotic pathways. Analysis of the bovine genome sequence identified orthologues of granzymes A, B, H, K and M, as well as another gene O, most closely related to granzyme A. The genes were found within 3 loci in the genome. Using specific PCR assays, all of these granzymes were shown to be expressed in Theileria-specific CD8+ T cells. Further studies were undertaken to study the role of granzyme B in killing. DNA constructs encoding functional and non-functional forms of bovine granzyme B were produced and the proteins expressed in COS cells were used to establish an enzymatic assay to detect and quantify expression of functional granzyme B protein. Using this assay, the levels of killing of different T. parvaspecific CD8+ T cell clones were found to be significantly correlating with levels of granzyme B protein expression. Moreover, the granzyme B inhibitor III, Z-IETDFMK was shown to inhibit killing by CD8+ T cell clones.
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2

Tinangon, Maria M. "Strategies to identify granzyme J /". abstract and full text PDF (UNR users only), 2001. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1404986.

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Koot, Gretchen E. "Serine and cysteine protease inhibitors for blockade of cell mediated cytotoxicity /". abstract and full text PDF (UNR users only), 2002. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3121138.

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Ben, Safta Thouraya. "Implication de la protéine suppresseur de tumeurs p53 dans la mort cellulaire induite par les lymphocytes T cytotoxiques et les cellules NK : rôle dans la régulation de l’apoptose dépendante du granzyme B". Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS162/document.

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Les lymphocytes T cytotoxiques (CTL) et les cellules tueuses naturelles (NK) éliminent leurs cellules cibles tumorales grâce à l’exocytose et à la libération du contenu des granules cytotoxiques contenant une protéine formant des pores, appelée perforine (PFN), et une famille de serine-protéases induisant la mort cellulaire, appelés granzymes (Gzms). Ces Gzms, pénètrent dans les cellules cibles de manière dépendante de la PFN et activent diverses voies de signalisation apoptotiques aboutissant à la mort de la cellule cible. Au cours de ce travail, nous avons étudié le rôle de la protéine suppresseur de tumeurs p53 dans la cascade moléculaire conduisant à l’apoptose induite par les effecteurs cytotoxiques via la voie PFN/Granzyme B (GzmB). Nous avons ainsi pu montrer qu’en réponse au GzmB ou à des effecteurs cytotoxiques, la forme sauvage de p53 s’accumule dans les cellules cibles au niveau des mitochondries afin d’interagir avec la protéine anti-apoptotique Bcl-2 et de réguler positivement la perméabilisation de la membrane mitochondriale externe induite par le GzmB. L’activité non transcriptionelle de p53 au niveau des mitochondries joue donc un rôle clé dans le contrôle de l’apoptose induite par les CTL et les NK (Ben Safta et al. J Immunol 2015). Etant donné que le gène TP53 est muté dans plus de 50% des tumeurs humaines, nous avons également cherché à déterminer si la restauration d’une p53 sauvage dans des cellules tumorales portant une p53 non fonctionnelle pourrait potentialiser la réponse cytotoxique antitumorale. Nos résultats montrent qu'effectivement, la réactivation pharmacologique de l’activité sauvage de p53 dans une lignée d'adénocarcinome mammaire possédant une p53 mutée sensibilise ces cellules tumorales à la lyse induite par les cellules NK via l’activation d’un processus d’autophagie et d’une cascade d’événements moléculaires qui sont en cours d’identification
Cytotoxic T lymphocytes (CTL) and natural killer (NK) cells eliminate their tumor target cells through exocytosis and release of the cytotoxic granules (CG) content. These CG contain a pore-forming protein called perforin (PFN), and a family of cell death inducing serine-proteases, called granzymes (Gzms). Gzms enter the target cells in a PFN-dependent manner and activate various apoptotic signaling pathways leading to the death of the target cell. In this work, we studied the role of the tumor suppressor protein p53 in the molecular cascade leading to apoptosis induced by cytotoxic effectors via the PFN/Granzyme B (GzmB) pathway. We have shown that in response to GzmB or to cytotoxic effectors, wild-type p53 accumulates on target mitochondria in order to interact with the anti-apoptotic protein Bcl-2 and to positively regulate the GzmB-induced mitochondrial outer membrane permeabilization. Thus, the non-transcriptional activity of p53 in the mitochondria plays a key role in the control of apoptosis induced by CTL and NK (Ben Safta et al J Immunol 2015). Because the TP53 gene is mutated in more than 50% of human tumors, we also aimed to determine whether the restoration of a wild-type p53 fonction in tumor cells carrying a non-functional p53 could potentiate the cytotoxic antitumor response. Our results show that the pharmacological reactivation of a wild-type p53 activity in a mammary adenocarcinoma cell line harboring a mutated p53 sensitize these tumor cells to the NK cell lysis via the activation of autophagy and a cascade of molecular events that are being identified
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LAFAURIE, CLOTILDE. "Etude de la regulation de la transcription et de l'expression des genes des granzymes b et h humains". Paris 11, 1997. http://www.theses.fr/1997PA112327.

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Les granzymes sont une famille de serine esterases exprimee de facon specifique dans les lymphocytes t actives. Nous avons etudie la regulation de l'expression des granzymes b et h humains. Deux axes ont ete choisis : la caracterisation des evenements genetiques necessaires a la regulation de l'expression de ces deux genes dans les lymphocytes t actives et l'etude de l'expression des proteines codees par ces deux genes dans differentes populations cellulaires. Nous avons caracterise un promoteur minimal qui controlait specifiquement la transcription du gene du granzyme b dans les lymphocytes t cytotoxiques. Ce promoteur contient des sites specifiques des proteines ap-1, cbf et ikaros qui sont necessaires a l'activation de la transcription du gene du granzyme b. Nous avons utilise ce modele pour etudier le mecanisme utilise par la dexamethasone pour inhiber l'expression du gene du granzyme b. Nous avons mis en evidence que cette inhibition etait transcriptionnelle et impliquait l'inhibition de la liaison des facteurs de transactivation sur les sites ap-1 et ikaros. Nous avons montre que la dexamethasone etait capable d'inhiber l'expression nucleaire des isoformes actives d'ikaros. Nous avons caracterise une region d'adn en amont du site de l'initiation de la transcription du gene du granzyme h responsable de l'expression specifique de ce gene dans les cellules yt-2c2. Cette region est capable de lier une proteine nucleaire specifiquement exprimee dans les noyaux des cellules yt-2c2. Nous avons montre que le granzyme b etait exprime dans des cellules non t. Nous avons produit un anticorps monoclonal dirige contre le granzyme h afin d'etudier son expression.
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6

Mouchacca, Pierre. "Granzyme B-td TOMATO, un nouvel outil fluorescent pour le suivi de la cytolyse chez la souris". Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4008/document.

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La fonction de cytolyse est un mécanisme majeur des effecteurs du système immunitaire pour éliminer les cellules infectées ou tumorales. Cette fonction associe l'activité de la perforine, qui forme des pores dans la membrane d'une cellule cible, à la sécrétion de protéases: les granzymes. Ces dernières sont des molécules pro-apoptotiques qui induisent la mort de la cellule cible. Les granzymes et en particulier granzyme B ciblent plusieurs voies intracellulaires complémentaires pour assurer l'efficacité de la cytolyse. Or il est difficile d'observer directement la fonction de cytolyse au cours de réponse immunitaire in vivo dans des conditions physiologiques. Dans les travaux présentés dans cette thèse, nous avons développé un nouveau modèle qui permet de suivre la fonction de cytolyse en temps réel par l'expression d'une protéine de fusion fluorescente GZMB-tdTomato. Les résultats obtenus par expression rétrovirale ont montré que la protéine de fusion est correctement exprimée dans les vésicules cytolytiques qui deviennent fluorescentes. Dans un second temps, nous avons réalisé un nouveau modèle murin qui exprime GZMB-tdTomato de manière substituée au GZMB natif par recombinaison homologue (Knock In). Nous avons mis en évidence que la protéine de fusion conserve l'activité catalytique de la protéine native et ses caractéristiques (conditions d'expression, de maturation, de sécrétion et demeure active après le passage dans la cellule cible lors de la cytolyse). En utilisant un modèle murin exprimant un TCR transgénique nous avons pu suivre le déroulement de la fonction de cytolyse de lymphocytes cytotoxiques en temps réel par video microscopies
Cytolysis is a major function used by the immune system's effectors to kill infected or tumor cells. Cytolysis depends on the pore forming protein perforin and the secretion of proteases of the granzyme family. Granzymes, including granzyme B (GZMB) have pro-apoptotic features and induce target cell death. Several complementary pathways are triggered by granzymes to ensure efficient cytolysis. It remains difficult to directly observe cytolysis during in vivo immune responses under physiological conditions. In this PhD we developed a new model to visualize cytolytic function in real time by expression of a fusion protein: GZMB-tdTomato. Results obtained from retroviral transduction showed that the fusion protein is correctly expressed in cytolytic vesicles, which became fluorescent. We then constructed a new mouse model by homologous recombination (Knock In) that express GZMB-tdTomato substituted for the native GZMB. The fusion protein conserves the catalytic activity of GZMB and its features (expression, maturation, secretion conditions) and remains active after its passage into target cells. Using TCR transgenic OTI cells, we followed the sequence of events of cytolysis from lymphocytes in real time by videomicroscopy. We also observed the cytolytic vesicles relocalization towards the cell contact zone and the death of target cell by cytolysis. Finally, we studied in vivo differentiation of naïve lymphocyte to cytolytic effector cells (the acquisition of cytolysis) and target cell death after bacterial infection
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Sumaria, Nital. "The relevance of specific molecular and cellular effectors during murine cytomegalovirus infection". University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0116.

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[Truncated abstract] The design and development of effective anti-viral immunotherapies requires a comprehensive understanding of the cellular and molecular processes that are involved in the generation and regulation of immune responses. The fundamental objective of the immune system is to successfully complete the task of eliminating/controlling the invading pathogen without causing overt pathology. Cytomegaloviruses (CMVs) are large DNA viruses that are able to evade immune attack and persist lifelong within the host. In a healthy host, CMV causes an asymptomatic infection, but in instances of decreased immune functions, such as in newborns, acquired immunodeficiency syndrome (AIDS) patients and transplant recipients, the infection can result in serious morbidity and mortality. Thus, human CMV (HCMV) is a clinically important pathogen and an understanding of the pathogenesis, mechanisms of immune subversion and, importantly the cascade of immune events that ensue following infection is highly relevant. The studies presented in this thesis have provided useful insight into various aspects of viral immunity and it is hoped that they will assist in the design of more effective therapies against viruses of clinical importance. Genetic variability in humans can greatly influence anti-viral immune responses and the outcome of viral infection. ... Furthermore, these studies provide novel evidence that NK cells are also crucial for the control of virus in some organs of susceptible mice during early acute infection. The data reveals that both NK cells and CD8+ T cells utilise perforin- and IFN-? dependent control of MCMV. Furthermore, these studies provide novel evidence that protection mediated by Ly49H+ NK cells in resistant mice is dependent on perforin. Chapter 3 focuses on the biological relevance of Grz during MCMV infection. These studies found that GrzA and GrzB are essential components of the machinery involved in limiting MCMV during acute infection. These analyses also provide the first evidence suggesting that GrzM plays a role, albeit minor, in controlling MCMV replication. Furthermore, the current studies suggest that Grz can mediate direct antiviral activities independent of the induction of cell death in conjunction with perforin. Interestingly, in the absence of both GrzA and GrzB (GrzAB), mice were as susceptible to MCMV infection as perforin-deficient mice. However, unlike perforin-deficient mice, GrzAB-deficient mice controlled and survived the infection. In Chapter 4 the roles of perforin, GrzA and GrzB in anti-viral immunity and immunopathology during MCMV infection were examined. These studies show that NK cell-derived perforin is required to eliminate infected targets as well as activated effector cells, suggesting that NK cells are crucial not only in defensive immunity but also in limiting the immune activation that follows MCMV infection. In summary, the studies presented in this thesis define the significant role played by specific effector molecules in limiting MCMV replication during different stages of this viral infection. Furthermore, these studies provide novel evidence that perforin, GrzA and GrzB play distinct roles in defensive immunity and limiting immunopathology during MCMV infection.
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Benechet, Alexandre. "Dynamic of the effector T cells egress from secondary lymphoid organs after infection". Paris 7, 2014. http://www.theses.fr/2014PA077126.

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Une réponse immunitaire efficace va dépendre de la migration des cellules immunitaires à l'intérieur et entre les tissus lymphoïdes. Notre compréhension des facteurs impliqués dans la migration des lymphocytes T effecteurs antigen-spécifiques après une infection reste incomplète. La sortie des T effecteurs du ganglion drainant est une des étapes essentielles dans l'éradication potentielle du virus au site de l'infection. Bien qu'il soit connu que le récepteur au shingosine-1- phosphate (S1PR1) contrôle la sortie des T naïfs, son influence sur l'émigration des T effecteurs après infection reste obscure. Dans cette étude, nous avons dans un premier temps utilisé la technique de marquage au complexe d'histocompatibilité majeur (CHM) Tétramérique in-situ, ainsi que l'imagerie intra vitale d'un modèle de souris rapporteur granzyme B (GzmB) YFP afin de décrire le panel migratoire des T antigène-spécifiques dans le ganglion drainant après une infection virale localisée. Les T effecteurs localisent premièrement au paracortex tôt après l'infection puis enfin migrent à la périphérie du ganglion. Une fois en périphérie, les effecteurs vont emprunter les sinus lymphatiques corticaux ainsi que medullaires pour émigrer du ganglion. De plus, afin d'investiguer le role de S1PR1 dans la dynamique des T effecteurs nous avons développé une souris déficiente spécifiquement dans les T effecteurs dont la délétion est contrôlée dans le temps après infection. En utilisant ce modèle unique nous avons clairement démontré que même, en l'absence de signaux de rétention comme CCR7 et CD62L, S1PR1 est le signal essentiel à la sortie des T effecteurs du ganglion drainant
An effective immune response depends on the large-scale, but carefully regulated migration of cells within and between lymphoid tissues. Our understanding of the factors that regulate the anatomical program followed by antigen-specific T cells during an infection remains incomplete. Egress of effector T cell from the draining lymph node (dLN) is one of the essential steps for the eventual eradication of the pathogen at the infection site. Although it is known that sphingosine-1-phosphate receptor 1 (S1PR1) controls naive T cell exit, how S1PR1 influences the emigration of effector T cells after infection is not well understood. Herein, by using both in-situ major histocompatibility complex (MHC)-tetramer staining and intravital imaging of a granzyme B (GzmB) YFP reporter mouse, we mapped the endogenous antigen-specific CD8 T cell response after localized viral infection in the dLN. In fact, we observed the localization of effector T cells in the paracortex early after infection, followed by the migration to the periphery. Notably, they exit the dLN via the medullary and cortical lymphatic sinuses. Furthermore, to assess the role of S1PR1 in their dynamic behavior, we generated a conditional GzmB YFP deficient mice to disrupt S1PR1 signals specifically and temporally in effector CD8 T cells after infection. Using this unique model we clearly demonstrate that after infection, even in the absence of retention signals such as CCR7 and CD62L S1PR1 signaling is the overriding factor that regulates effector T cell emigration from the dLN
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Chollat-Namy, Marie. "Effet de l’inactivation du gène suppresseur de tumeur p53 et de sa réactivation pharmacologique sur la réponse cytotoxique anti-tumorale The Pharmalogical Reactivation of p53 Function Improves Breast Tumor Cell Lysis by Granzyme B and NK Cells Through Induction of Autophagy Mutant P53 Gain of Function Stimulates PD-L1 Expression". Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL032.

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Le système immunitaire joue un rôle important dans le contrôle et l'éradication du cancer. Des acteurs majeurs de la réponse immune antitumorale sont les cellules tueuses naturelles (ou cellules NK) et les lymphocytes T cytotoxiques (ou CTL), capable de reconnaitre et détruire des cellules tumorales par l’exocytose de perforine et de granzymes contenus dans leur granule cytotoxique. Il a été montré au sein du laboratoire l’implication de la protéine suppresseur de tumeur p53 dans cette voie apoptotique. Or, plus de 50% des tumeurs humaines présentent des mutations inactivatrices de p53 ce qui favorise le développement tumoral. De ce fait, l’inactivation fréquente de p53 dans les tumeurs humaines pourrait leur permettre d’échapper à la destruction par les CTL et les cellules NK.Dans ce contexte, mes travaux de thèse ont montré que la réactivation pharmacologique de la fonction de p53 sauvage dans des cellules tumorales exprimant une p53 mutée augmente leur susceptibilité à la lyse induite par les cellules NK grâce à l’induction d’un processus d’autophagie. De plus, j’ai cherché à déterminer le lien entre les mutations de p53 et l’expression à la surface des cellules tumorales de PD-L1 qui empêche l’activation optimale des cellules cytotoxiques et conduit à leur épuisement. Mes travaux actuels suggèrent que l’expression de p53 mutantes induits une surexpression de PD-L1 à la surface des cellules cancéreuses. Les mécanismes expliquant ce phénomène sont en cours d’études
Immune system plays an important role in the control and destruction of cancer cells. The major effectors of antitumor immune response are Natural Killer (NK) cells and the cytotoxic T lymphocytes, which recognize et destroy tumor cells by exocytosis of perforin and granzymes contained in cytotoxic granules. It has been previously shown in the laboratory that the tumor suppressor p53 plays an important role in this apoptotic pathway. However more than 50% of human tumors have p53 inactivating mutations which favor tumor development. Consequently, frequent p53 inactivation in human tumor could enable them to escape from destruction by cytotoxic immune cells. In this context, my thesis work has shown that the pharmacological reactivation of wild type p53 function in cancer cells expressing a mutated p53 increased their susceptibility to NK cell-mediated apoptosis cells through the induction of an autophagic process. Moreover, I tried to determine the link between p53 mutations and the expression of the immune checkpoint ligand PD-L1 which prevent efficient activation of cytotoxic cells and promote immune cells exhaustion. My work suggests that the expression of p53 mutants promotes an the expression of PD-L1 at the cancer cell surface. The study of the underlying mechanisms is still in progress
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Musembi, Susan Mbithe. "Immunological assays relevant to definition of bovine theileria parva-specific cytotoxic CD8+ T cell responses". Thesis, Brunel University, 2012. http://bura.brunel.ac.uk/handle/2438/7171.

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A major objective in Theileria parva subunit vaccine development is to induce a vaccine antigen specific response mediated by cytotoxic CD8+ T cells (CTL). Therefore it is essential to be able to measure the frequency of the responding CD8+ T cells after vaccination and correlate it with a clinical outcome on challenge. Recently concluded immunogenicity and efficacy studies of T. parva specific CTL antigens showed successful induction of CTL responses in some animals, which correlated with reduced disease severity after challenge. To provide correlates of immunity antigen-specific CD8+ T cell mediated IFN-γ responses and CTL lytic responses were measured over the course of the experiments. Several challenges presented in these trials aimed at optimising vaccine efficacy. While the IFN-γ ELISPOT is a sensitive and reliable assay widely used in vaccine research, the use of chromium/indium release assay remains to be the only assay in use that measures T. parva-specific CTL activity. Hence the overall goal of the study was to develop novel reagents and novel assays to identify parasite-specific CD8+ T lymphocytes with lytic potential. To address this objective, bovine perforin, granzymes A and B, as specific effector proteins expressed in activated CTL were cloned and expressed using a baculovirus expression system. Sequence analysis of the cloned cDNAs showed the isolated cDNA belonged to the perforin and granzyme sub-families respectively. Perforin cDNA demonstrated 85% homology to human perforin with presence of conserved regions resembling calcium binding motif, membrane attack complex component as well complement protein. The sequences encoded by the cloned granzyme A and B cDNAs have the features of a trypsin like serine protease and demonstrates over 70% homology to the human cDNA over the active enzyme region as well catalytic residues characteristic of serine proteases. The expressed polypeptides of all three proteins were used to produce specific antibodies for use as reagents in immunoassays including ELISpot and intracellular staining for flow cytometric analysis. While the antibodies showed reactivity to the recombinant proteins, these reagents displayed different functionality in the recognition of the native protein. Peptide-major histocompatibility complexes (MHC) class I tetrameric complexes (tetramers) are proving invaluable as fluorescent reagents for enumeration, characterisation and isolation of peptide-specific CD8+ T cells and have afforded advantages to phenotype antigen-specific T cells with minimal in vitro manipulation. Fluorescent bovine tetramers were shown to specifically stain antigen-specific CTL by directly binding the T cell receptor (TCR). Analyses of CD8 T-cell responses in live-vaccine immunised cattle also showed that this method is robust and demonstrates changes in the kinetics and specificity of the CD8+ T cell response in primary and secondary infections with T. parva. On average, results of functional assays and tetramer staining followed parallel trends, measured roughly the same populations and allowed for surface and intracellular staining for CD8 T cell marker and perforin, respectively, demonstrating a method that reliably quantifies the frequency, phenotype and function of specific CD8+ T cells. The technical simplicity, rapidity and ability of the flow cytometric technique described in this thesis to measure low frequency antigen-specific responses suggests that tetramer staining, combined with functional assays could be broadly applicable to the valuation of vaccination efficacy to determine which protocols are most successful in inducing CTL responses.
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Części książek na temat "Granzymes"

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Greenberg, A. H., i D. W. Litchfield. "Granzymes and Apoptosis: Targeting the Cell Cycle". W Pathways for Cytolysis, 95–119. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79414-8_6.

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Haddad, Patrick, Dieter E. Jenne, Olivier Krähenbühl i Jürg Tschopp. "Structure and Possible Functions of Lymphocyte Granzymes". W Cytotoxic Cells: Recognition, Effector Function, Generation, and Methods, 251–62. Boston, MA: Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-6814-4_23.

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Noonan, Janis, i Brona M. Murphy. "Cytotoxic T Lymphocytes and Their Granzymes: An Overview". W Resistance to Targeted Anti-Cancer Therapeutics, 91–112. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17807-3_5.

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Kuppili, Raja Reddy, i Kakoli Bose. "Calpains and Granzymes: Non-caspase Proteases in Cell Death". W Proteases in Apoptosis: Pathways, Protocols and Translational Advances, 53–94. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19497-4_3.

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Jenne, D. E., i J. Tschopp. "Granzymes: a Family of Serine Proteases in Granules of Cytolytic T Lymphocytes". W Current Topics in Microbiology and Immunology, 33–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73911-8_4.

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Coughlin, Paul, Emma Morris i Lynne Hampson. "The role of granzymes and serpins in regulating cell growth and death". W Programmed Cell Death in Animals and Plants, 55–64. London: Garland Science, 2021. http://dx.doi.org/10.1201/9781003076889-5.

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Gooch, Jan W. "Granzyme". W Encyclopedic Dictionary of Polymers, 896. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13866.

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Gressner, A. M., i O. A. Gressner. "Granzyme". W Springer Reference Medizin, 1027. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1332.

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Gressner, A. M., i O. A. Gressner. "Granzyme". W Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_1332-1.

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León, Diego López, Isabelle Fellay, Pierre-Yves Mantel i Michael Walch. "Killing Bacteria with Cytotoxic Effector Proteins of Human Killer Immune Cells: Granzymes, Granulysin, and Perforin". W Methods in Molecular Biology, 275–84. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6673-8_18.

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Streszczenia konferencji na temat "Granzymes"

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Ngan, DA, SV Vickerman, PR Hiebert, H. Zhao, WM Elliott, JC Hogg, DJ Granville, SP Man i DD Sin. "The Role of Granzyme B in the Pathogenesis of COPD." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2961.

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Wiles, Andrew, Claire Hoptay, Matthew Sharron, Mayya Geha, Kanneboyina Nagaraju i Robert J. Freishtat. "Sepsis-Related Mortality Is Reduced In The Absence Of Granzyme B". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4677.

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Vickerman, SV, H. Zhao, Y. Li, DA Ngan, PR Hiebert, DJ Granville, SF Man i DD Sin. "Characterization of Granzyme B Protein Expression in Blood from COPD Patients." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2941.

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Sharron, Matthew, Andrew A. Wiles, Angela S. Benton i Robert J. Freishtat. "Mechanisms Of Platelet Granzyme B Induced End-Organ Apoptosis In Sepsis". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6151.

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Xu, L., F. Hu, X. Liu, L. Zhu, L. Ren, H. Liu, H. Zhu i Y. Su. "AB0102 Impairment of granzyme b-producing regulatory b cells exacerbated rheumatoid arthritis". W Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2269.

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Sharron, Matthew, Andrew A. Wiles, Claire E. Hoptay, Kanneboyina Nagaraju i Robert J. Freishtat. "Platelet Granzyme B Induces Contact-Dependent End-Organ Apoptosis During Murine Sepsis". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6009.

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Kim, Won Dong, Kang Hyeon Choe, Yeon Mok Oh, Sang Do Lee, Kyu Rae Kim, Hyun Sook Chi i James C. Hogg. "Granzyme B Positive Cells Outnumber CD8+ Cells In Small Airways Of Centrilobular Emphysema". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5803.

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Barczyk, A., E. Sozanska i W. Pierzchala. "Increased Expression of Granzyme B, but Not Perforin in CD8+ Cells in Sarcoidosis." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3185.

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Wroblewski, Mark A., Raimund Bauer, Miguel Cubas Córdova, Florian Udonta, Isabel Ben Batalla, Victoria Gensch, Stefanie Sawall i in. "Abstract 3253: Mast cell-derived granzyme b contributes to resistance against anti-angiogenic therapy". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3253.

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Shevtsov, Maxim, Susanne Kaesler, Stefan Stangl, Luidmila Yakovleva, Ruslana Tagaeva, Yaroslav Marchenko, Boris Nikolaev i in. "Abstract 2878: Granzyme B functionalized nanocarriers targeting membrane-bound Hsp70 for multimodal cancer therapies". W Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2878.

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