Dissertations / Theses on the topic 'Granzymes'
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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.
Full textTinangon, 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.
Full textKoot, 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.
Full textBen, 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.
Full textCytotoxic 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
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.
Full textMouchacca, 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.
Full textCytolysis 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
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.
Full textBenechet, Alexandre. "Dynamic of the effector T cells egress from secondary lymphoid organs after infection." Paris 7, 2014. http://www.theses.fr/2014PA077126.
Full textAn 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
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.
Full textImmune 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
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.
Full textBruno, Alain. "Effets cellulaires des rayonnements ionisants sur les cellules hématopoïétiques immatures." Paris 11, 2000. http://www.theses.fr/2000PA11T021.
Full textUsing cell lines representative of hemopoietic differentiation, we showed that immature hemopoietic CD34+ cells are less sensitive to ionizing radiation than mature CD34- cells. Ln immature cells, ionizing radiation activate apoptotic cell death related to neutra! sphingomyelinase stimulation responsible for nuclear sphingomyelin hydrolysis and nuclear ceramide generation. Ln CD34+ cells, ionizing radiation do not produce neither ceramide nor apoptosis, and activate delayed reproductive cell death (mitotic cell death). These results suggest that nuclear neutra! sphingomyelinase plays a pivotai role in the cellular response of ionizing radiation. Ln a second part, we tried to determine the mecanisms responsible for negative regulation of nuclear sphingomyelinase in CD34+ cells. We first considered nuclear proteolytic events. Thus, we provided evidences for the presence of the serine-protease, Granzyme B, in the nucleus of CD34+ cells. We showed that ionizing radiation up-regulates Granzyme B expression both in the nucleus and the cytoplasm of these cells. This overexpression is not responsible for the lack of apoptotic response of CD34+ cells to ionizing radiation. Lnterestingly, we observed that Granzyme B overexpression confers a potent cytotoxic ability to these cells towards target cell lines of myeloid and lymphoid origin. Our results suggest that when irradiated, CD34+ cells acquire cytotoxic potential toward cells of the medullar environment. Conversely, in cytotoxic T lymphocytes, ionizing radiation triggers down-regulation of Granzyme B expression correlated with the loss of cytotoxic function. These results suggest immunosuppressor effects of ionizing radiation, related to their capacity to modulate Granzyme B expression
HADDAD, PATRICK. "Etude de la structure et de la regulation de genes codant pour des serine esterases (granzymes a et h) chez l'homme : relations a la cytotoxicite a mediation cellulaire et applications a la clinique." Paris 7, 1990. http://www.theses.fr/1990PA077202.
Full textHariss, Fatima. "Etude du rôle des Lymphocytes Intraépithéliaux innés dans la réponse immune protectrice contre Cryptosporidium parvum." Thesis, Université de Lille (2018-2021), 2021. http://www.theses.fr/2021LILUS047.
Full textIntraepithelial lymphocytes (IEL) reside between intestinal epithelial cells and thus are the first immune cells to contact intestinal pathogens. In addition to respond rapidly to infection, they regulate intestinal homeostasis and maintain the epithelial barrier. This wide range of functions is achieved by distinct subsets of T and innate lymphocytes. Innate IEL which share many features with NK/ILC1 cells have been identified recently. These cells dominate the gut epithelium at birth and when the adaptive immunity is compromised. Their role in the immune response against intestinal pathogens remains however poorly studied.During my PhD thesis, I have investigated the role of innate IEL subsets in Crysptosporidium infection. Crysptosporidium is a common parasite that infects the gut epithelium. The infection is self-limiting in immunocompetent individuals, but it can be severe in immunocompromised individuals and children in whom innate IEL dominate.To study the specific role of innate IEL, we have developed an in vitro model that consist to co-culture mice 3D intestinal organoids infected with C parvum with innate IELs from RAG2-/- mice. Thanks to this original model, we demonstrated that innate IELs control parasite proliferation. We further showed that although innate IEL secrete IFN-ƴ in response to C parvum infection, the IFN-ƴ secretion was not sufficient to inhibit parasite proliferation. The protective effect of innate IELs was in fact mediated by a cytotoxic, granzyme-dependent mechanism. Moreover, transcriptomic analysis revealed that infected epithelial cells down regulated serpinb9b, a granzyme inhibitor, and thus may be more sensitive to cytotoxic attack
Boivin, Wendy Anne. "Extracellular granzyme B and pathophysiological implications." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42827.
Full textHiebert, Paul Ryan. "Granzyme B in skin aging, injury and repair." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44226.
Full textHendel, Alon. "Granzyme B in vascular remodeling and pathological angiogenesis." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44782.
Full textEstébanez, Perpiñá Eva. "Crystal Structure of Human Granzyme B. Modelling of the Granzyme B-Cation-Independent Mannose-6-Phosphate Receptor Complex. Crystal Structure of Human Pro-Granzyme K. Crystal Structure of the Procarboxypeptidase from Helicoverpa armigera." Doctoral thesis, Universitat Autònoma de Barcelona, 2002. http://hdl.handle.net/10803/3477.
Full textGranzima B es la proteina prototípica de la familia de serina proteasas que se encuentran en células NK y CTLs. GzmB induce apoptosis mediante activación de las caspasas, y está implicada en la etiología de la artritis reumatoidea. Hemos cristalizado y resuelto la estructura 3D de la GzmB humana a una resolución de 3.1Å. GzmB muestra un plegamiento similar al de catepsina G y quimasa humanas. GzmB exhibe una especificidad de substrato muy inusual ya que corta tras Asp, debido a la presencia de Arg226 en bolsillo de especificidad S1. El sitio de unión del substrato está diseñado para acomodar y cortar hexapéptidos, i.e. IETD_SG, secuencia presente en el lugar de activación de la caspasa-3 y de Bid, sus substratos fisiológicos. Esta estructura ayudará en el diseño de inhibidores que podrian ser usados en la cura de enfermedades inflamatorias crónicas.
Granzyme B y el Receptor Manosa-6-Fosfato Independiente de Cationes
GzmB cristalizó como dímero, mediante la interdigitación de las cadenas de azúcares unidas a Asn65 en los dos monómeros. GzmB es captada por las células mediante el Receptor Manosa-6-Fosfato Independiente de Cationes. Sugerimos que la GzmB dimérica sea la forma internalizada por las células diana. Hemos modelado cómo posiblemente GzmB se une a su receptor celular.
Estructura Tridimensional de pro-Granzyme K humana
Hemos determinado la estructura 3D de la pGzmK a una resolución de 2.2Å. pGzmK se parece más a una serina proteasa activa, a pesar de ser un zimógeno. Esta proteina carece de triada zimogénica y utiliza un nuevo mecanismo de estabilización de la forma inactiva.
Estructura Tridimensional de una Procarboxipeptidasa de Helicoverpa armigera. H. armigera es un insecto cuya plaga afecta a un gran número de países. Hemos determinado la estructura 3D de una nueva carboxipeptidasa (PCPAHa) de larvas de H. armigera, la primera resuelta de un insecto hasta la fecha. El zimógeno de PCPAHa muestra una estructura similar a las ya resueltas de mamífero. Su sitio de activación presenta el motivo (Ala)5Lys. Es curioso apreciar similar motivo ((Ala)6Lys) cerca del extremo N-terminal del enzima activo. Ser255 agranda el bolsillo S1´de especificidad y influencia las preferencias de substrato de ésta enzima. Hemos modelado el extremo C-terminal del LCI dentro del sitio activo de PCPAHa.
Crystal Structure of Human Granzyme B
Granzyme B is the prototypic member of the granzymes, trypsin-like serine proteinases localized in activated NK cells and CTLs. GzmB triggers apoptosis by activating the caspases, and is implicated in the etiology of rheumatoid arthritis. Human GzmB has been crystallized and its structure has been determined to 3.1 Å resolution. GzmB overall fold is similar to that found in cathepsin G and human chymase. GzmB exhibits an unusual substrate specificity as it cleaves after Asp residues due to the presence of Arg226 at the back of the S1-specificity pocket. GzmB substrate binding site is designed to fit and cleave hexapeptides, i.e. IETD_SG, sequence present in the activation site of caspase-3 and Bid, physiological substrates of GzmB. This structure would help in the design of inhibitors for a treatment of chronic inflammatory disorders.
Granzyme B and the Cation-Independent Mannose-6-Phosphate Receptor
Our crystal structure of GzmB unexpectedly revealed a dimer, mediated by the interdigitation of the sugar chains attached to Asn65 in the two monomers. The uptake of GzmB is effected by the cation-independent mannose-6-phosphate (M6P) receptor. We suggest that the GzmB dimer would be the form preferentially recognized by its receptor. To investigate the probable binding mode of GzmB to its cell receptor we have modeled the binding of the GzmB dimer to the M6P-receptor.
Crystal Structure of Human Pro-Granzyme K
We have determined the crystal structure of human pGzmK at 2.2 resolution. The overall fold of pGzmK is most similar to that found in active serine proteinases rather than in zymogens. An unusual feature of pGzmK is that the residues Ser32, His40 and Asp194 do not form a zymogen triad, while pGzmK uses a novel mechanism for zymogen stabilization.
Crystal Structure of a Procarboxypeptidase from Helicoverpa armigera
H. armigera is one of the most serious insect pests worldwide. We present the 2.5 Å crystal structure from this novel procarboxypeptidase (PCPAHa) from H. armigera larvae, the first one reported for an insect. PCPAHa zymogen has a 3D structure similar to the corresponding mammalian digestive carboxypeptidases. The activation site contains the motif (Ala)5Lys. It is noteworthy the occurrence of the same (Ala)6Lys near the C-terminus of the active enzyme. Ser255 enlarges the S1' specificity pocket and influences the substrate preferences of the enzyme. The C-terminal tail of LCI was modeled into PCPAHa active site.
Fellows, Edward. "Granzyme H: A novel cell-death-inducing serine protease." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-78190.
Full textChamberlain, Ciara M. "Granzyme B in abdominal aortic aneurysm and aortic dissection." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/5584.
Full textPinkoski, Michael J. "The role of granzyme B in target cell apoptosis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23057.pdf.
Full textUhl, Dieter. "Einfluss körperlicher Ausdauerbelastung auf Perforin und Granzyme-B-exprimierende Lymphozytenpopulationen." [S.l.] : [s.n.], 2002. http://www.freidok.uni-freiburg.de/volltexte/440.
Full textAng, Lisa Shouning. "The extracellular role of granzyme B in abdominal aortic aneurysm." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45649.
Full textTrzaska, Timo [Verfasser]. "The role of granzyme B in antigen-presenting cells / Timo Trzaska." Ulm : Universität Ulm, 2021. http://d-nb.info/1234554968/34.
Full textHirst, Claire Elizabeth 1971. "Tissue distribution and regulation of the granzyme B inhibitor, proteinase inhibitor 9." Monash University, Dept. of Biochemistry and Molecular Biology, 2002. http://arrow.monash.edu.au/hdl/1959.1/8488.
Full textBabichuk, Charolyn Kim. "Transcriptional regulation of the murine granzyme B gene in cytotoxic T cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq22945.pdf.
Full textHaeryfar, Seyed Mohammad Mansour. "Antiestrogens modulate the perforin/granzyme pathway of natural killer cell-mediated cytolysis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0001/MQ45052.pdf.
Full textBannard, Oliver Michael. "The memory functions of CD8⁺ T cells that have expressed granzyme B." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611596.
Full textYokoi, Akiko. "Selective Expression and Function of Granzyme D in the Lymphohematopoietic Stromal Cells." Kyoto University, 2000. http://hdl.handle.net/2433/181270.
Full textSchiffer, Sonja [Verfasser]. "Improving the therapeutic potential of human granzyme B and evaluation of granzyme M as novel effector molecules in cytolytic fusion proteins for the treatment of Serpin B9-positive cancer / Sonja Schiffer." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2014. http://d-nb.info/1048671534/34.
Full textDhenni, Rama B. S. "Role of Granzyme B in the Susceptibility to Secondary Bacterial Infection after Viral Infection." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1460446984.
Full textMerkulova, Yulia. "Granzyme B inhibits keratinocyte migration by disrupting epidermal growth factor receptor (EGFR)-mediated signaling." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/58050.
Full textMedicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
Sharma, Mehul. "Extracellular Granzyme K mediates endothelial inflammation through the cleavage of Protease Activated Receptor-1." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/55402.
Full textMedicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
Schwesinger, Elisabeth [Verfasser]. "Charakterisierung Granzym-B-sezernierender B-Zellen / Elisabeth Schwesinger." Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1020022434/34.
Full textPanitz, Verena Michaela [Verfasser]. "Regulation of human granzyme B-producing plasmacytoid dendritic cells by viral stimuli / Verena Michaela Panitz." Ulm : Universität Ulm, 2017. http://d-nb.info/1122644876/34.
Full textSeignez, Cédric. "Etude des mécanismes d'action d'une immunothérapie par un lipide A, seul ou associé à l'oxaliplatine, dans des modèles de cancers coliques." Thesis, Dijon, 2013. http://www.theses.fr/2013DIJOMU01/document.
Full textColorectal cancer is a major public health concern in France. Resistance to standard chemotherapy requires development of novel therapeutic approaches. In the past decades, our team showed the immunotherapeutic properties of lipid A in a model of colon cancer in rats. 95% of rats bearing small carcinomas were cured following treatment by lipid A. The study of mechanisms underlying this immunotherapy allowed us to show that the antitumor effect of lipid A was dependent on cytotoxicity induced by granzyme B produced by intratumoral neutrophils. Indeed, we have shown that, in the tumor microenvironment, neutrophils produced granzyme B and had a pro-tumorigenic N2 phenotype. When rats were treated with lipid A, neutrophils shifted to an antitumor N1 phenotype and released granzyme B, thus inducing apoptosis of tumor cells. In rats bearing advanced carcinoma, the effectiveness of lipid A was reduced and only 40% of animals were cured. An injection of oxaliplatin prior to lipid A treatment allowed sustaining the effectiveness of lipid A immunotherapy. In the present study, we showed that oxaliplatin injection induced tumor cell senescence. The microenvironment produced by senescent cells enabled then the recruitment of neutrophils within tumors, subsequently activated by lipid immunotherapy.Combining the induction of tumor cells senescence and activation of immune cells by an immunotherapeutic agent constitute an original and interesting therapeutic approach, but still studies must be carrying out to better understand underlying mechanisms
Hirayasu, Hirofumi. "Studies on the role of a lymphocyte protease granzyme A in the intestinal epithelial-cell turnover." Kyoto University, 2010. http://hdl.handle.net/2433/131909.
Full text0048
新制・論文博士
博士(農学)
乙第12509号
論農博第2743号
新制||農||986(附属図書館)
学位論文||H22||N4574(農学部図書室)
28300
京都大学大学院農学研究科食品生物科学専攻
(主査)教授 伏木 亨, 教授 井上 國世, 教授 安達 修二
学位規則第4条第2項該当
Pashkovska, N. V. "The role of perforin/granzyme-induced apoptosis in the development of cognitive impairment in diabetes mellitus." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18836.
Full textDahlke, Karen [Verfasser]. "Die regulatorische Rolle Granzym B-sezernierender B-Lymphozyten / Karen Dahlke." Ulm : Universität Ulm. Medizinische Fakultät, 2013. http://d-nb.info/1036454460/34.
Full textNishie, Mariko. "Downregulated ATP6V1B1 expression acidifies the intracellular environment of cancer cells leading to resistance to antibody-dependent cellular cytotoxicity." Kyoto University, 2021. http://hdl.handle.net/2433/261614.
Full textNgan, David Allen. "Discovering inflammatory biomarkers in chronic obstructive pulmonary disease and cystic fibrosis : a case study of granzyme B." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/36292.
Full textAl, Absi Antoun. "Role of the actin cytoskeleton in breast cancer cell resistance to natural killer cells." Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ038/document.
Full textTumor immune evasion plays a central role in cancer progression and is a major hurdle to effective immunotherapy. In this Thesis, we examine the role of the actin cytoskeleton in breast cancer cell resistance to natural killer (NK) cell-mediated cell lysis. We found that resistant breast cancer cells escape from NK-cell attack through a rapid and prominent accumulation of actin near the immunological synapse, a process we termed the “actin response”. Our mechanistic investigations suggest that the actin response drives autophagosome polarization toward the immunological synapse and thereby facilitates the autophagy-mediated degradation of NK cell-derived cytotoxic molecules such as granzyme B. In addition, the actin response was associated with inhibitory ligand clustering at the immunological synapse, suggesting that it is a common driver of different immune evasion mechanisms. Taken together, our data lays the groundwork for therapeutic approaches aimed at interfering with the actin response and restoring an effective anti-tumor immune response
Vargas, Hernández Giovanni [UNESP]. "Linfomas cutâneos em cães: estudo epidemiológico, morfológico, imunofenotípico e seroproteico." Universidade Estadual Paulista (UNESP), 2017. http://hdl.handle.net/11449/151209.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
O linfoma cutâneo (LC) em cães é uma doença que se caracteriza pela proliferação clonal de linfócitos atípicos na pele (MILLER et al., 2013). É um linfoma não-Hodgkin, formado por um grupo de doenças neoplásicas malignas de linfócitos T e B e células Natural Killer (NK), cuja primeira manifestação clínica é a presença de lesões cutâneas, sem existir lesão extra cutâneas no momento do diagnóstico (RUEDA; CORTES, 2008). A apresentação clínica é inespecífica e pode mimetizar muitas dermatites (FONTAINE et al., 2010). Nas fases inicias da doença torna-se difícil diferenciar a condição neoplásica de quadro inflamatório linfocítico cutâneo (MURPHY; OLIVRY 2000). Descrita pela primeira vez em 1972 (KELLY et al., 1972), e para muitos autores a doença rara e de etiologia desconhecida (FONTAINE et al., 2009; WITHROW et al., 2013). Diversos estudos mencionaram novas variedades e formas de apresentação do LC na espécie canina baseadas principalmente nos resultados de reações imuno-histoquímicas, comportamento clínico da neoplasia e nas frequentes mudanças da classificação desta doença na espécie humana, que tem levado na classificação em novas variantes de LC (WILLEMZE et al., 2005; DE BOSSCHERE; DECLERCQ, 2008; AFFOLTER et al., 2009; FONTAINE et al., 2009; MILLER et al., 2013; MOORE et al., 2012). Nas últimas três décadas, a classificação morfológica e imunofenotípica do LC em medicina veterinária baseou-se nos critérios de classificação utilizados em humanos (VALLI et al., 2011). O objetivo desta revisão é definir quais são as atuais variantes, tipos e subtipos do LC em cães e estabelecer as principais semelhanças e diferenças com a classificação existente na espécie humana.
Cutaneous lymphoma (LC) in dogs is a disease characterized by the clonal proliferation of atypical lymphocytes in the skin (Miller et al., 2013). It is a non-Hodgkin's lymphoma, consisting of a group of malignant neoplastic diseases of T and B lymphocytes and Natural Killer (NK) cells, whose first clinical manifestation is the presence of cutaneous lesions, with no extra-cutaneous lesion at the time of diagnosis (WHEEL . The clinical presentation is non-specific and may mimic many dermatitis (FONTAINE et al., 2010). In the early stages of the disease, it is difficult to differentiate the neoplastic condition of cutaneous lymphocytic inflammatory disease (MURPHY; OLIVRY 2000). It was first described in 1972 (KELLY et al., 1972), and for many authors, the rare disease of unknown etiology (FONTAINE et al., 2009, WITHROW et al., 2013). Several studies have mentioned new varieties and forms of LC presentation in the canine species based mainly on the results of immunohistochemical reactions, clinical behavior of the neoplasia and the frequent changes in the classification of this disease in the human species, which has led to classification in new variants of LC (Muller et al., 2009), and in the literature on the use of this method (Macker et al., 2009). In the last three decades, the morphological and immunophenotypic classification of CL in veterinary medicine was based on the classification criteria used in humans (VALLI et al., 2011). The objective of this review is to define the current variants, types and subtypes of LC in dogs and establish the main similarities and differences with the existing classification in the human species.
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