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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
211

Characterization of the Anti-Tumour Immune Response Following Treatment with an Infected Leukemia Cell Vaccine

Dempster, Holly January 2018 (has links)
Current treatment methods for Acute Leukemia (AL) only provide temporary therapeutic efficacy as most patients will experience relapse within 2 years following first remission. Our lab has determined that vaccination with autologous cells infected with oncolytic virus MG1 can provide durable cures in a pre-clinical mouse model of AL. However, the mechanism(s) by which the infected cell vaccine (ICV) stimulates T cell dependent anti-tumour immunity and provides protection against tumour growth is unknown. This thesis was aimed to determine 1) what antigen presenting cell populations are activated post ICV immunization and 2) what T cell subsets are important in developing anti-tumour immunity during ICV immunization. My thesis has demonstrated that ICV immunization is more effective at inducing in vivo dendritic cell activation compared to irradiated L1210 cells alone and this activation may be a reason as to why we see improved anti-tumour efficacy in our ICV model. In addition, we have determined that CD4 T cells play an essential anti-leukemic role during ICV immunization and that neutralizing antibody production is a CD4 T cell dependent mechanism. Our data also demonstrates that both CD4 and CD8 T cell populations from ICV immunized mice provide a leukemia-specific anti-tumour immune response. Taken together, this data suggests that CD4 T cells may be acting as helper T cells to aid in the robust activation of leukemia-specific anti-tumour CD8 T cells. Our pre-clinical data characterizing the immune response has improved our understanding of the mechanism(s) which contribute to the efficacy of the ICV and will help provide a rationale framework with which to begin translating this treatment to clinical trials.
212

Immunothérapie et métabolisme tumorale / Clinical amplification of NK cells : effect of metabolism

Belkahla Benamor, Sana 11 October 2017 (has links)
La formation et le développement d’une tumeur sont provoqués par une série de défauts qui se produisent à l'intérieur de la cellule cancéreuse et dans son microenvironnement. Ces anomalies permettent à la cellule de développer ses propres stratégies de croissance, de prolifération, de différenciation et de métabolisme.La modification du métabolisme respiratoire, est l'une des stratégies utilisée par les cellules cancéreuses favorisant la fermentation lactique au lieu de la phosphorylation oxydative OXPHOS (respiration). Cette adaptation métabolique porte le nom d’effet Warburg.Nous avons proposé un concept thérapeutique novateur basé sur l'induction de changements métaboliques par l'utilisation de dichloroacétate (DCA) associée avec l'immunothérapie en utilisant les cellules NK activées. Le DCA, molécule inhibitrice de la PDK, induit l'activation de la PDH, responsable de la catalyse de pyruvate en Acétylcoenzyme A (Ac-CoA), favorise alors l’oxydation du glucose dans la mitochondrie. Le DCA a déjà été utilisé depuis longtemps comme traitement hypocholestérolémiant et bloquant l’acidose lactique. Mon équipe a montré auparavant que le changement métabolique permet aux cellules tumorales d'échapper à la réponse immune.Nous avons observé que le traitement par DCA induisait, dépendante du phénotype p53, une forte up-régulation de l'expression du mRNA et des protéines de stress MICA, MICB et ULBP1, ligands spécifiques des récepteurs activateurs NKG2D des cellules NK, et induise alors une réponse cytotoxique contre les cellules tumorale.D'autre part nous avons évalué l'effet de DCA sur l'expression des transporteurs ABC qui interviennent dans l'efflux des agents anticancéreux utilisé dans la chimiothérapie. L'expression des transporteurs ABC était fortement liée aux phénotypes de chimiorésistance. Nous avons bien confirmé que le DCA provoque une diminution de l'expression de ABCB1, ABCC1, ABCC5 et ABCG2 dans les cellules wtp53 alors qu'il induit une augmentation dans les cellules mutantp53 ou nullp53.Les promoteurs des transporteurs et les protéines de stress étudiés comportent également plusieurs sites de liaison spécifique au facteur de transcription MEF2, qui est la cible d’ERK5. Nous avons bien constaté que en plus de ca capacité de changer le métabolisme tumorale, le DCA modifie l'expression ABCB1, ABCC1, ABCC5 et ABCG2 par l'activation de la voie ERK5/MEF2 .Ces résultats sont confirmé dans diverses lignées cellulaires, ainsi que dans des cellules issues de patients et dans un modèle in vivo / Tumorigenesis is caused by a series of defects that occur within the cancer cell and its microenvironment. These abnormalities allow the tumor cell to develop its own strategies for growth, proliferation, differentiation and metabolism. In the last, cancer cells favor lactic fermentation instead of oxidative phosphorylation OXPHOS (respiration). This metabolic adaptation is called the Warburg effect.We proposed an innovative therapeutic concept based on the induction of metabolic changes by the use of dichloroacetate (DCA) and this is associated with immunotherapy using activated NK cells. DCA, a pyruvate dehydrogenase kinase (PDK) inhibitor, induces the activation of pyruvate dehydrogenase (PDH), responsible for the catalysis of pyruvate to acetylcoenzyme A (Ac-CoA), promoting the oxidation of glucose/pyruvate in the mitochondria. DCA has been used for a long time as a cholesterol-lowering and anti-lactic acidosis therapy. My team has previously shown that the metabolic change allows tumor cells to escape the immune response. I have observed that DCA treatment induced a high upregulation of mRNA and protein expression of the stress ligands MICA, MICB and ULBP1. These are recognized by the NK cell activating receptor NKG2D, inducing a NK cell-mediated cytotoxic response against tumor cells. DCA-induced expression of these stress ligands depends on wtp53 expression on the tumor cell.On the other hand, we evaluated the effect of DCA on the expression of ABC carriers, which intervene in the efflux of anticancer agents used in chemotherapy. The expression of ABC carriers is strongly related to drug resistance phenotypes. We observed that DCA causes a decrease in the expression of ABCB1, ABCC1, ABCC5 and ABCG2 in wtp53 cells while it induces an increase in mutantp53 or nullp53 cells. Conversely, DCA-induced accumulation of antitumor drugs, i.e. daunorubicin, and favors chemotherapy-induced tumor death only in wtp53-expressing cancer cells. The promoters of these ABC transporters and the stress proteins presented above contain several binding sites specific to the transcription factor MEF2, which is the target of ERK5. We have found that in addition to the ability to change tumor metabolism, DCA modifies the expression ABCB1, ABCC1, ABCC5 and ABCG2 by activation of the ERK5 / MEF2 pathway. These results are confirmed in various cell lines, in cells derived from patients and in an in vivo model
213

Développement de nouvelles approches thérapeutiques dans la lutte contre les infections à arénavius : vaccination et immunothérapie passive / Development of new therapeutic approaches in the fight against arenavirus infections : vaccination and passive immunotherapy

Zaza, Amélie 25 January 2018 (has links)
La famille des Arenaviridae comporte sept virus responsables de fièvres hémorragiques humaines. Ces virus représentent un risque naturel pour les populations vivant dans les zones endémiques, ou y séjournant comme les militaires français déployés. Ce risque peut également toucher des populations vivant en dehors des zones endémiques en raison du risque d'importation d'un patient infecté ou consécutivement à l'utilisation intentionnelle et malveillante de tels virus dans le cadre d'une attaque bioterroriste. Les fièvres hémorragiques humaines causées par les arénavirus sont relativement rares et les premiers symptômes, non spécifiques, sont souvent confondus avec ceux de maladies plus fréquentes dans ces régions, comme le paludisme ou les arboviroses. Par conséquent, le diagnostic clinique est souvent retardé, ce qui réduit l'efficacité du seul traitement étiologique actuellement préconisé, la ribavirine. Dans ce contexte, le développement de solutions prophylactiques similaires au vaccin Candid #1, protégeant contre l'arénavirus Junin, constituent une alternative intéressante. Dans le cadre du développement de candidats vaccins, la première stratégie utilisée dans ce travail a consisté à atténuer la pathogénicité du virus d'intérêt en ciblant une étape clé de la réplication des arénavirus. Nous avons choisi l'étape du bourgeonnement viral, dont l'acteur principal est la protéine Z. Une preuve de concept a été réalisée avec le virus de la chorioméningite lymphocytaire (LCMV). Pour cela, nous avons conçu un système de génétique inverse qui exprime un segment L viral où le gène de la protéine Z est remplacé par un gène d'intérêt. De manière surprenante, ce virus recombinant était capable de produire en culture cellulaire une progénie à un titre très faible sans l'apport en trans de la protéine Z. Nous avons identifié des domaines tardifs dans la séquence peptidique de la nucléoprotéine, motifs peptidiques permettant le détournement de la machinerie cellulaire impliquée dans la production d'exosomes et présents dans les protéines de matrices virales, comme la protéine Z des arénavirus. Nous avons observé que ces domaines pourraient partiellement compenser l'absence de la protéine Z. Des résultats similaires ont été obtenus avec deux autres arénavirus ayant une importance majeure en santé publique, les virus Lassa et Machupo, tous deux responsables de fièvres hémorragiques humaines. Cette suppression pourrait constituer une stratégie d'atténuation et semblerait prometteuse en vue du développement de candidats vaccins réplicatifs atténués. En effet, elle pourrait être utilisée sur plusieurs arénavirus responsables de pathologies humaines. Une approche complémentaire à cette stratégie vaccinale a été envisagée. Dans le but de développer un traitement d'urgence, utilisant des immunoglobulines équines hautement purifiées, les F(ab')2, selon la méthodologie de la société Fab'entech, deux études préliminaires ont été réalisées. La première a permis de vérifier la capcité des virus à se répliquer dans les cellules immunitaires circulantes de cheval. La seconde a permis l'évaluation du cahier des charges qualité de particules virales en vue de leur utilisation comme source d'antigène afin de produire les F(ab')2. Une seconde stratégie vaccinale a été envisagée, basée sur une modification du nombre de segments génomiques viraux. Des travaux précédents ont montré qu'un arénavirus à 3 segments, au lieu de 2, était viable et atténué, tout en pouvant exprimer 2 gènes d'intérêt supplémentaires. Cette stratégie a été utilisée sur le virus Machupo, responsable de fièvres hémorragiques en Bolivie. Ce virus recombinant devrait exprimer les glycoprotéiques tronquées des virus Chapare et Guanarito. Ce candidat vaccin a été caractérisé en culture cellulaire, et a induit une protection de 50% des animaux lors d'une administration en post-exposition [etc...] / The Arenaviridae family comprises seven viruses responsible for human hemorrhagic fevers. These viruses represent a natural threat to the local populations, healthcare workers and scientists, as well as to the French forces deployed in the regions where these viruses are endemic. This viral threat can also be intentional in case of a bioterrorist attack. Human hemorrhagic fevers caused by arenaviruses are relatively rare and the first symptoms, frequently non-specific, are often confused with more common diseases such as malaria. Therefore, their diagnosis is delayed, which reduces the efficacy of ribavirin, the only etiological treatment currently recommended. ln this context, the development of prophylactic treatments, such as the Candid #1 vaccine targeting the Junin arenavirus, are an interesting alternative. The first strategy developed in this work to produce a vaccine candidate relied on the attenuation of the virus of interest by targeting a key stage of its replication. We chose the egress step, in which the main actor is the Z protein. This work was conducted using the lymphocytic choriomeningitis virus (LCMV). We therefore designed a reverse genetic system, and replaced the Z gene by the fluorescent protein eGFP reporter gene. Surprisingly, during its cellular infection, a progeny was detected in absence of the Z protein trans-complementation although the titer remained very low. ln this infectious model, we further identified late motifs in the nucleoprotein genome, comparable to those known in the Z protein. These NP late motifs seemed to play an essential role in the compensation of the absence of the Z protein. Similar results were observed using two others arenaviruses of medical importance, the Lassa and Machupo viruses, responsible of human hemorrhagic fevers. The strong diminution of the resulting vaccine candidate replication suggests that this strategy would render safe enough BSL-4 viruses to be used as a multivalent vaccine platform in humans. A complementary approach has been studied in this work. ln order to develop an emergency treatment, based on the production of highly purified F(ab')2 equine immunoglobulins, according to the Fab'entech technology. Two preliminary studies were carried out. The first one consisted in the study of the replication of arenaviruses in circulating horse's white blood cells. The second tested the specifications of attenuated viral particles that could be used as an antigen source to produce the F(ab')2 under good manufacturing practices. Another vaccine strategy was developed using the previously described duplication of the LCMV S genomic small segment in order to produce a tri-segmented recombinant virus. This genetic modification, known to attenuate the LCMV virus pathogenicity, allows the expression of two genes of interest. This strategy has been applied onto the South American Machupo virus, responsible for hemorrhagic fevers in Bolivia. A recombinant Machupo virus was designed to express the truncated glycoproteins of the Chapare and Guanarito viruses, two other New World mammarenaviruses responsible of human hemorrhagic fevers. This vaccine candidate was characterized in cell culture, and showed a 50% post-exposure protective effect in the animal model used. Taken together this work led to the development of two vaccine strategies and to the identification of a promising source of antigens to be used to produce highly purified F(ab')2 polyclonal immunoglobulin, which is the first step to the development of an emergency treatment
214

The co-localization of tissue kallikrein and transforming growth factor - beta 1 in the non-cancerous and cancerous kidney

Moodley, Rumesha January 2003 (has links)
Submitted in part fulfillment for the Degree of Master of Technology: Biotechnology, Durban Institute of Technology, 2003. / Evidence suggests that the induction of tissue kallikrein, and the subsequently formed kinins, enhances proliferation of tumour cells because of their mitogenic property. Additionally, the kinin peptides are believed to promote the invasion of normal tissue by tumour cells. TGF-l is a potent inhibitor of the growth of renal epithelial cells, and is a classical anti-mitogen, which is central to many of its antiproliferative effects. No studies thus far have been performed, as to whether the proposed anti-mitogenesis ofTGF-1 has a regulatory effect on the cell proliferative action of kinins on renal epithelial and carcinoma cells. / M
215

The Role of CD8+ T Cell Phenotype and Cytotoxicity on Cancer Immunotherapy

Stark, Felicity January 2011 (has links)
Cancer vaccines can fail despite the induction of large numbers of CD8+ T cells. Two categories of memory CD8+ T cells have been defined; central memory (TCM, IL-7RαhighCD44highCD62Lhigh) and effector memory (TEM, IL-7RαhighCD44highCD62Llow). It is clear that the memory phenotype of CD8+ T cells can affect vaccine potential; however methods to augment a beneficial phenotype are not clear. I have compared three vaccine delivery systems: Listeria monocytogenes, Salmonella enterica serovar Typhimurium and the particulate liposomal adjuvant, archaeosomes, for their efficacy to protect against murine melanoma. My study revealed that the anti-tumour response is strongly influenced by the kinetics, phenotype, and lymph node homing potential of CD8+ T cells. Listeria monocytogenes-ovalbumin (LM-OVA) induced TCM cells were adept at long lasting protection against B16-OVA melanoma due to their increased homeostatic and antigen-induced proliferation, interleukin-2 production, and ability to extravasate into tumour draining lymph nodes. Conversely, although Salmonella Typhimurium-ovalbumin (ST-OVA) induced TEM, produced IFN-γ, and killed target cells, this was insufficient for long-term tumour protection. Selectin-ligand engagements of TCM cells influenced their homing potential and efficacy against murine melanoma. Fucosyltransferase deficient (FtDKO) mice, lacking functional selectin ligands, were vaccinated with LM-OVA; despite the activation of cytotoxic CD8+ T cells, there was a reduced protection against murine melanoma compared to wild-type. FtDKO CD8+ T cells exhibited reduced extravasation into FtDKO lymph nodes compared to wild-type. Additionally, fewer FtDKO CD8+ T cells compared to wild-type migrated into tumour sites. Archaeosome vaccination was used to compare the influence of CD8+ T cell quantity versus phenotype. Single or multiple therapeutic vaccinations with archaeosome-OVA yielded transient melanoma tumour protection, despite an increased frequency of circulating and tumour infiltrating CD8+ T cells. This correlated with increased expression of Program death receptor-1 (PD-1) on CD8+ T cells and induction of regulatory T cells. Prophylactic archaeosome-OVA vaccination resulted in a maximal frequency of antigen-specific CD8+ T cells of ~50-60 % with just three injections, and ~50 % of the mice were of mice were afforded long-term tumour protection (> 90 days). Overall, my study shows that the choice of vaccine adjuvant and/or vector can profoundly influence CD8+ T cell quality and cancer vaccine efficacy.
216

Targeting Tumour Vasculature with Oncolytic Viruses

De Silva, Naomi Samantha January 2014 (has links)
Oncolytic viruses (OVs) have been engineered or selected for cancer cell-specific infection; however, we have found that following intravenous administration of vesicular stomatitis virus (VSV), tumour cell killing rapidly extends far beyond the initial sites of infection. This Bystander Effect is due to the virus’ ability to specifically target tumour vasculature through tumour-specific infection of tumour endothelium and the induction of an inflammatory response resulting in tumour-restricted coagulation, acute vascular disruption, apoptosis and necrosis of the tumour core. VSV-infected tumours, reconstructed in three-dimensions from serial histological sections, revealed that the majority of the tumour mass lacks significant blood flow in contrast to uninfected tumours, which exhibit relatively uniform perfusion. VSV infection rapidly induced intravascular coagulation within 6 hours of intravenous administration. The induction of coagulation was dependent on neutrophils and could be prevented with inhibitors of the coagulation pathway. Normal vasculature was not infected by VSV and no increase in coagulation was observed. Vascular collapse was also observed with the oncolytic poxvirus, JX-594, in patients and preclinical models. Biopsies from patients enrolled in a dose escalation trial for JX-594 were immunoreactive for vaccinia antigens and transgene products in high dose cohorts. Tumour-associated vessels from patients treated with JX-594 were infected with JX-594 and expressed virally encoded transgenes. A decrease in blood flow was also observed 5 days post infection. Several viruses, VSV, JX-594, vvDD, Maraba, and Sindbis, were able to rapidly induce widespread bystander cell death in a subset of mouse models. Tumours responded to OV therapy in three ways, and the type of response was determined by two factors - susceptibility to infection and the heterogeneity of the tumour microenvironment. Heterogeneity correlated with E-cadherin expression. Among tumours that supported viral replication, cancers with low E-cadherin expression were susceptible to vascular collapse. E-cadherin positive tumours were susceptible to infection and direct cell killing but resistant to vascular disruption or bystander cell death. If poorly-differentiated tumours were resistant to infection, no acute cell killing was observed. These histological subtypes provide a potential framework for the rational selection of patients, the integration of combination therapies and the creation of designer viruses to improve the success of OV therapy.
217

Engineering Novel TNFα-armed Oncolytic Viruses for Combination Immunotherapy with SMAC Mimetics

Pichette, Stephanie January 2016 (has links)
Small molecular Inhibitor of Apoptosis (IAP) antagonists, known as Smac mimetic compounds (SMCs), are a novel class of anti-cancer drugs currently undergoing clinical trials. SMCs were designed to mimic the function of the pro-apoptotic protein, Smac, which directly depletes cells of cIAP1 and cIAP2, and consequently renders tumour cells sensitive to death in the presence of proinflammatory ligands such as TNFα. The Korneluk lab recently reported that SMCs synergize with the attenuated oncolytic virus Vesicular stomatitis virus (VSVΔ51) by eliciting an enhanced immune response in mice, such that the combined therapy is vastly superior to stand-alone therapies. To improve on this SMC-mediated synergistic response, I generated variants of TNFα-armed VSVΔ51. Due to high ectopic expression of TNFα in infected cells, a five times lower viral dose of TNFα-armed VSVΔ51 combined with SMC treatment was sufficient to improve the survival rate as compared to SMC and VSVΔ51 co-therapy. This improved synergistic response is attributed to a bystander effect whereby the spread of TNFα from infected cells leads to the death of neighbouring, uninfected cells in the presence of a SMC. In addition, the double treatment induced vasculature collapse in solid tumours, revealing another mechanism by which cytokine-armed VSVΔ51 in combination with a SMC can induce cancer cell death. This approach demonstrates great potential for engineered oncolytic virus and SMCs as a new combination immunotherapy for cancer treatment.
218

Identification et caractérisation d'une population de cellules lymphoïdes innées de type 2 (ILC2) associée à la sévérité de la rhinite allergique et de l'asthme / Identification and characterization of an ILC2 subset linked to allergic rhinitis and asthma severity

Beuraud, Chloé 08 December 2016 (has links)
Identification et caractérisation d'une population d'ILC2 associée à la sévérité de la rhinite allergique et de l'asthmeTrois catégories de cellules lymphoïdes innées (innate lymphoid cells, ILC) ont été décrites récemment sur la base de leurs phénotypes et leurs caractéristiques fonctionnelles : les ILC1, ILC2 et ILC3. Les ILC2 semblent avoir un rôle pro-inflammatoire important dans l’allergie en raison de leur capacité à produire de grandes quantités de cytokines TH2.Pour mieux comprendre le rôle de ces cellules dans l’allergie respiratoire, nous avons comparé les ILC sanguines de patients atteints d’une rhinite allergique associée ou non à un asthme, à celles de sujets non allergiques. Cette étude révèle de multiples différences fonctionnelles entre les ILC circulantes de sujets sains et allergiques. Notamment, la fréquence d’ILC2 exprimant le récepteur aux chimiokines CCR10 est augmentée dans le sang de patients asthmatiques sévères.CCR10 pouvant permettre le recrutement des ILC vers les organes cibles, le rôle des ILC2 CCR10+ dans la physiopathologie de l’asthme a été étudié. Leur présence dans les poumons humains a été observée. Des analyses fonctionnelles et phénotypiques ont révélé que cette sous-population cellulaire était peu activée mais présentait une plasticité leur conférant des caractéristiques proches des ILC1. La déplétion de ces cellules dans un modèle murin d’asthme allergique aggrave l’hyperréactivité bronchique.Les travaux de cette thèse documentent le rôle des ILC dans l’asthme. En particulier, la fréquence sanguine d’ILC2 CCR10+ augmente avec la sévérité de la maladie. Les résultats obtenus dans les modèles animaux suggèrent que ces cellules auraient un rôle bénéfique dans le contrôle de l’asthme. La voie du CCR10 pourrait représenter une nouvelle cible pour le développement de traitements innovants contre l’asthme ou une source prometteuse de biomarqueurs. / Identification and characterization of an ILC2 subset linked to allergic rhinitis and asthma severityInnate lymphoid cells (ILCs) have been classified into ILC1, ILC2 and ILC3 subsets based on their respective phenotypes and functions. Considering the strong ability of ILC2s to produce TH2 cytokines, these cells likely play a significant role in allergic diseases.To better understand the role of these cells in respiratory allergies, we compared blood ILCs from allergic patients with or without asthma to non-allergic individuals. Together our results show multiple functional differences between ILC from allergic and healthy subjects. In particular, ILC2s expressing the chemokine receptor CCR10 are specifically enriched in the blood of patients with severe allergic asthma.Considering that CCR10 could allow the recruitment of ILCs to target organs, the role of CCR10+ ILC2s in asthma physiopathology has been studied. This ILC2 subtype is present in human lungs. Functional and phenotypic analyses revealed that these cells are less activated than other ILC2s and show ILC1-like properties. CCR10+ ILC2s depletion in a mouse model of allergic asthma exacerbate airway hyperreactivity.Together, this work documents the role of ILCs in asthma. Specifically, circulating CCR10+ ILC2 frequency increases with asthma severity. The results obtained in mouse models suggest that these cells could have a beneficial role in asthma control. CCR10 pathway could represent a new target to elaborate breakthrough treatments against asthma or a source of promising biomarkers.
219

Induction of Human Pluripotent Stem Cell-Derived Natural Killer Cells for Immunotherapy under chemically defined condition / ヒト多能性幹細胞由来Natural killer細胞を用いた既知組成条件での免疫療法の開発

Matsubara, Hiroyuki 25 November 2019 (has links)
付記する学位プログラム名: 充実した健康長寿社会を築く総合医療開発リーダー育成プログラム / 京都大学 / 0048 / 新制・課程博士 / 博士(医科学) / 甲第22121号 / 医科博第106号 / 新制||医科||7(附属図書館) / 京都大学大学院医学研究科医科学専攻 / (主査)教授 濵﨑 洋子, 教授 河本 宏, 教授 生田 宏一 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
220

High Frequency Production of T Cell-Derived iPSC Clones Capable of Generating Potent Cytotoxic T Cells / T細胞から作製したiPS細胞は高頻度で強力なキラーT細胞を再生する能力を有する

Nagano, Seiji 23 March 2020 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第22347号 / 医博第4588号 / 新制||医||1042(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 生田 宏一, 教授 江藤 浩之, 教授 濵﨑 洋子 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

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