Tesi: "GM-CSF" – Grafiati

1

Bailie, Karen Elizabeth Margaret. "G-CSF and GM-CSF : effects on neonatal neutrophils". Thesis, Queen's University Belfast, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.482043.

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2

Chevalier, Anne Sophie. "Utilisation thérapeutique du G-CSF et du GM-CSF en hématologie". Paris 5, 1993. http://www.theses.fr/1993PA05P248.

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3

Hallsworth, Matthew Pearce. "GM-CSF and eosinophil survival in asthma". Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341883.

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4

Bernstone, Laura. "Characterisation of HIV-1 infection and M-CSF and GM-CSF macrophages". Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.572833.

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Macrophages are a natural target cell for HIV-1 infection, and they contribute to the development of disease as they are important for transmission, dissemination and persistence of the virus in an infected patient. Macrophages are less well-studied than T cells and cell lines in relation to HIV-1 infection, yet macrophages are highly specialised and key aspects of the HIV-1 life cycle in these cells are already known to differ compared to other cell types. HIV-1 entry into macrophages has been suggested to occur by macropinocytosis, however the entry route in these cells has not been fully characterised. In this thesis I have tested a panel of pharmacological inhibitors of cellular proteins and uptake pathways, in order to delineate the requirements for HIV-1 entry into macrophages and to determine the nature of the entry route. My findings suggest that the following host factors are important for entry; membrane cholesterol, actin rearrangements, dynamin, sodium-hydrogen exchange, Pak1, and Rac. Other factors including clathrin, PI-3 kinase, Rho kinase and some isoforms of PKC were found to be dispensable for infection or to inhibit infection. Macrophages are a heterogeneous group of cells, and tissue macrophages from different parts of the body differ in their morphology, phenotype and function. I have used the growth factors M-CSF and GM-CSF to direct monocytes to differentiate into distinct types of macrophage. This allowed me to determine that different macrophages differ in their susceptibility to infection and in their ability to support replication. This is likely to be due to variation in HIV-1 receptor expression and the levels of key HIV-1 transcription factors, respectively. Overall this thesis contributes to existing knowledge regarding HIV-1 infection of macrophages. These findings may assist with the design of entry inhibitors, and with therapies designed to eradicate HIV-1 from infected individuals.

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5

Lin, Tony Wei Ting. "The role of GM-CSF/G-CSF & BKLF in the development of atherosclerosis". Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/10407.

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The studies described in this thesis are aimed to investigate the role of the pro-inflammatory cytokine GM-CSF/G-CSF, transcriptional factor KLF3 and psychological stress in KLF3 deficiency mice on neointimal formation, a common feature of atherosclerosis with the aid of perivascular collar model on murine model. The present study supports an important role for GM/CSF-G/CSF and KLF in atherosclerosis. There is now overwhelming evidence that the monocyte/macrophage has a crucial role in the initiation and progression of atherosclerotic plaque and this has led to the view that the recruitment and activity of these cells may represent important therapeutic targets. Atherosclerosis is multi-factorial and well-established risk factor include: hypertension, hypercholesterolemia, diabetes, smoking and aging (Altman 2003), increasing evidence suggest an important role for psychological factor (stress) in the development of CHD. Furthermore, accumulating evidence suggests that GM-CSF/G-CSF and KLF3 has protective effect against atherosclerosis. The studies described in this thesis investigated on the effect of the pro-inflammatory cytokine (the role of GM-CSF/G-CSF and KLF3) and the psychological factor (stress and the role KLF3) factors on neointimal formation, a common feature of atherosclerosis. The experimental models of neointimal formation play an important role in understanding the pathogenesis of atherosclerosis (White, 1989), which could contribute to the development of therapeutic modalities and examining the effectiveness of potential interventions that target neointimal proliferative disease. Several mouse models of atherosclerosis have been employed experimentally worldwide. In this thesis murine perivascular collar placement around the femoral artery injury model was investigated for the neointimal formation. Chapter 3 describes the role of the pro-inflammatory cytokine GM-CSF/G-CSF in the pathophysiology of atherosclerosis. GM-CSF/G-CSF exhibits many biological functions including; mediation of inflammatory responses effects (Kleemann, Zadelaar et al. 2008). The role of GM-CSF/G-CSF in injury-mediated neointimal formation is complex. Moreover, the effect of atherosclerotic state on the role of GM-CSF/G-CSF in the acute injury model has not been previously explored. Our study demonstrated that GM-CSF/G-CSF deficiency resulted in delayed neointimal formation at an earlier examined time-point (2 weeks). Thus, it suggested that GM-CSF/G-CSF displayed a net pro-atherogenic effect in this model of perivascular collar endothelial injury. This information could be used for improved early detection, prevention and treatment of atherosclerosis. Chapter 4 describes the role of KLF3 on neointimal formation. KLF3 had profound effects on using in vitro and in vivo either in animal models or in human subject (Cao, Sun et al. 2010). KLF3 have potent effects in stimulating proliferation (Dang, Pevsner et al. 2000; McConnell and Yang 2010), maturation, and function of hematopoietic cells cytokines (Turner and Crossley 1999; Cao, Sun et al. 2010). KLF3 exhibits a myeloproliferative disorder suggests that KLF3 regulates important process involved in haematopoietic differentiation (Turner and Crossley 1999). The studies discussed here reveal that KLF3 deficiency can have profound effects on cell differentiation, and function in vitro and in vivo. In addition, correlating and contrasting KLF3 structure-function relationships in vascular biology may enable an improved understanding of their physiologic and pathologic functions. Our study demonstrated that KLF3 deficiency resulted in delayed neointimal formation at an earlier examined time-point (2 weeks), suggesting that KLF3 deficiency may showed a net pro-atherogenic effect in this model of perivascular collar endothelial injury. This knowledge might be used for improved early detection, prevention and treatment of atherosclerosis. Future investigations are required to further clarify the underlying mechanisms, and the potential therapeutic benefit on KLF3 deficiency treatment in vascular proliferative disorders. Chapter 5 describes the role of stress and KLF3 deficiency on neointimal formation. Accumulating evidence suggests an important role for psychosocial factors such as stress in the development of CHD (Rozanski, Blumenthal et al. 1999); however the role of psychological stress in early responses in injury-induced neointimal formation remains debate. KLF3 deficiency mice exhibit reduced detrimental effects of chronic stress by induces vascular inflammation (Liu, Wen et al. 2010; Lu, Haldar et al. 2010), and therefore provide a unique genetic animal model to gain insight into the effect of stress on the aetiology of atherogenesis. This study evaluated the effect of acute psychological stress mediated by physical restraint on neointimal formation, and these effects were further explored in the absence of KLF3 deficiency. Although KLF3 deficiency showed minor effects (reduced inflammation and vessel proliferation), it was not found to be protective against stress-mediated increase in neointimal formation. This study suggested that acute psychological stress contributes to the pathogenesis of vessel neointimal proliferative disorders. Precise underlying mechanisms involving stress and KLF3 deficiency in neointimal formation require further clarification. However, these findings have provided some valuable insight on the role of stress and KLF3 deficiency in vessel proliferative responses. Therefore, the role of KLF3 deficiency in stress and neointimal formation appears complex at early stage. Future studies on the effect of stress on hemodynamic responses and their role on neointimal formation can be further investigated with the perivascular collar endothelial collar model as well as their potential pharmacological modulation.

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6

Mirabella, Fabio. "Regulation of the human IL-3/GM-CSF locus". Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487744.

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The human Interleukin-3 (IL-3) and Granulocyte-Macrophage Colony-Stimulating-Factor (GM-CSF) genes are two closely linked cytokine genes that are located within a conserved cytokine gene cluster. They are expressed in an inducible tissue-specific manner in a variety of haemopoietic cell types, and they contribute to the regulation of inflammatory responses arid haemopoiesis. For this reason their expression is strictly regulated. The experiments in this thesis describe an investigation into the factors and DNA elements involved in the control and regulation of these genes during T cell development. They focus in particular on the roles that DNase I hypersensitive sites (DHSs) and the nuclear proteins CTCF and RAD21 play within the GM-CSF/IL-3 gene locus.

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7

Grant, Olivia M. "GM-CSF Stress-Induced Priming of the Dendritic Cell". Ohio Dominican University Honors Theses / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=oduhonors1449522036.

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8

Adkins, Karissa Kathleen 1971. "Glucocorticoid regulation of GM-CSF in bronchial epithelial cells". Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282844.

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Inflammation plays a central role in the pathogenesis of asthma. Glucocorticoids are first line antiinflammatory therapy in the treatment of asthma and are effective inhibitors of inflammatory cytokines. Clinical data demonstrate that granulocyte-macrophage colony-stimulating factor (GM-CSF) production by airway epithelial cells may be an important target of inhaled glucocorticoid therapy. In this study, the regulatory mechanisms of GM-CSF expression by interleukin-1β (IL-1β) and the synthetic glucocorticoid dexamethasone (DEX) were examined in the BEAS-2B human bronchial epithelial cell line. It is hypothesized that glucocorticoids inhibit GM-CSF production in these cells through transcriptional mechanisms involving induction of the NF-κB inhibitory protein, IκB-α. Treatment of the BEAS-2B cells with IL-1β induced GM-CSF protein and mRNA levels, and further investigation showed this induction was mediated through transcriptional mechanisms. DEX treatment of BEAS-2B cells inhibited IL-1β-induced GM-CSF protein and mRNA production. GM-CSF mRNA was rapidly degraded in these cells, and DEX treatment did not significantly affect this decay rate. These data suggest that dexamethasone repression of GM-CSF expression is mediated predominantly through transcriptional mechanisms. This study then examined expression of IκB-α in the BEAS-2B cells as a possible mechanism of glucocorticoid repression of GM-CSF. IκB-α RNA levels were minimally induced by DEX in these cells, but this did not result in concurrent induction of IκB-α protein. Additional analysis showed that DEX treatment of BEAS-2B cells did not prevent nuclear translocation of the NF-κB subunit p65, or IL-1β-induced degradation of IκB-α protein. From these data, this study concludes that induction of IκB-α is not a significant mechanism of glucocorticoid-mediated repression of GM-CSF in the BEAS-2B cells.

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9

Aziz, Khalil Abdul. "Influence of GM-CSF and G-CSF on the mutual interactions between platelets and neutrophils". Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241473.

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10

Osborne, Cameron Stuart. "Transcriptional regulation of the GM-CSF gene in T lymphocytes /". Title page, contents and summary only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09pho81.pdf.

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11

Yang, Nianji Eric. "THE ROLE OF GM-CSF IN MACROPHAGE POLARISATION IN RESPONSE TO TROPOELASTIN-COATED POLYETHYLENE IMPLANTS IN VIVO". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15866.

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Our previous studies have shown that the incorporation of tropoelastin (TE) improves the biocompatibility of silk fibroin and low density polyethylene (PE). With the coating or blending of tropoelastin, both biomaterials underwent a favourable foreign body inflammatory response. Macrophage is a key cell in the biomaterial-induced inflammation and can be polarized into two main phenotypes (M1/M2) capable of inducing either pro-inflammatory or anti-inflammatory cytokine profiles during host responses. The objective of the present study was to investigate the possible underling mechanism of the improved biocompatibility with tropoelastin coating in terms of macrophage response. The macrophage infiltration and polarization was evaluated in vivo using C57BL/6 (wide-type) mice (n=32) and granulocyte macrophage colony-stimulating factor knock out (GM-CSF-/-) mice (n=32). PE-only (n=8), plasma immersion ion implantation treated PE (PIII) (n=8), PIII with one layer TE coating PE (PIII+TE, n=8) and PIII with double layers TE coating PE (PIII+2TE, n=8) were implanted subcutaneously into the back of mice separately. However, the group of PIII+TE was excluded. Implants were harvested at weeks 1, 2, 4 and 8. In addition, GM-CSF-/- mice model was used to investigate whether GM-CSF was the key cytokine in the adjustment of foreign body reaction. Our results show that tropoelstin affects the macrophage response in host responses. PIII+2TE decreased the infiltrative numbers of macrophages (F4/80+ cells), and elevated the percentage of M2 cells (F4/80+Ym-1+Arg-1+ cells) compared to PE-only during the acute inflammation. In addition, lower levels of macrophages with higher proportion of M2 cells were observed in GM-CSF-/- mice among three biomaterials. Based on the previous results, this study further demonstrated that PE with PIII+2TE modification can mitigate inflammatory response, defined mainly by higher number of M2 cells in the capsule of implantation. It also indicated that the deficiency of GM-CSF influenced the infiltration and M2 polarisation of macrophage. In conclusion, tropoelastin was assumed to elevate M2 percentage at the site of implantation via downregulation of GM-SCF. However, further investigations are needed to elucidate the downstream of GM-CSF in the polarisation of macrophage.

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12

Eubank, Tim. "M-CSF and GM-CSF induce human monocytes to express either pro- or anti-angiogenic factors". The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1069772001.

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13

Eubank, Timothy D. "M-CSF and GM-CSF induce human monocytes to express either pro- or anti-angiogenic factors". Columbus, Ohio : Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1069772001.

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Thesis (Ph. D.)--Ohio State University, 2003.
Title from first page of PDF file. Document formatted into pages; contains xx, 168 p.; also includes graphics (some col.). Includes abstract and vita. Advisor: Clay B. Marsh, Biochemistry Program. Includes bibliographical references (p. 150-168).

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14

Pinder, Emma Muriel. "Does GM-CSF restore effective neutrophil function in critically ill patients?" Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3943.

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Nosocomial infection is an increasing problem worldwide associated with significant morbidity and mortality in addition to heightened healthcare costs. The problem is even greater on the intensive care unit (ICU) where up to 20 of patients develop a secondary infection during their admission. In an era of increasing antibiotic resistance alternative strategies to prevent nosocomial infection must be sought. The intensive care population are recognised to be at high risk of developing immune dysfunction during their critical illness and this has been shown to be associated with an increased risk of the development of ICU acquired infection (ICUAI). The neutrophil, in particular, is key in terms of the host response to bacterial and fungal infections and impairments in neutrophil function have been demonstrated in critically ill patients. Granulocyte-macrophage colony-stimulating factor has been shown to improve the phagocytic function of impaired neutrophils ex-vivo and has previously been demonstrated to restore immune competent levels of monocyte HLA-DR expression in critically ill patients. If GM-CSF were demonstrated to restore neutrophil phagocytic function in critically ill patients in whom its known to be impaired it may have a role in preventing the development of ICUAI. Our initial study sought to validate neutrophil CD88 expression as a surrogate marker for phagocytic function. The dose finding study which followed aimed to determine the optimum dose and duration of GM-CSF to be carried forward to a randomised controlled trial. Finally, the randomised controlled trial sought to investigate the hypothesis that GM-CSF could restore effective neutrophil function in critically ill patients. While no significant difference was seen in our primary endpoint of neutrophil phagocytic capacity, on day 2 following administration of GM-CSF, we believe a small but true biological effect was observed suggesting further study is warranted to investigate whether GM-CSF could reduce the risk of ICUAI.

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15

CARDONE, MARCO. "Il GM-CSF può promuovere il differenziamento di monociti umani in cellule dendritiche dotate di distinte proprietà immuno-stimolatorie e migratorie: ruolo dell'espressione del recettore del GM-CSF". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/546.

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Le cellule dendritiche mieloidi (DCs) e i macrofagi evolvono da un precursore comune. Comunque, è ancora poco chiaro quale siano i fattori che controllano il differenziamento dei monociti in DC o macrofagi. Noi abbiamo riportato che la densità di superficie della subunità α del recettore del GM-CSF (GM-CSFR) in monociti del sangue periferico umano varia tra i diversi donatori. Sebbene poi nessuna correlazione sia stata trovata tra l’entità di espressione del GM-CSFR e la capacità di monociti di differenziare in DC in presenza di GM-CSF e IL-4, l’espressione del GM-CSFR è stata vista però influenzare fortemente la generazione di cellule CD1a+ DC-like in assenza di IL-4. Le cellule CD1a+ generate in presenza del solo GM-CSF sono risultate esprimere le molecole CD40, CD80, MHC I and II, DC-SIGN, MR, CCR5 e mantenere in modo parziale il CD14. Queste stesse cellule sono state anche trovate capaci di indurre spontaneamente l’espansione di linfociti T CD4+ and CD8+ allogenici rilascianti IFN-gamma, e migrare in risposta alla CCL4 e alla CCL19. Dopo stimolazione con vari ligandi dei TLR, infine, esse sono state trovate acquisire caratteristiche fenotipiche di DC mature. La loro capacità allostimolatoria, invece, non è risultata ulteriormente incrementare a causa della produzione endogena di IL-10. Infatti, una più alta risposta proliferativa di cellule T e produzione di IL-12 da parte delle stesse DC-like attivate è stata osservata solo in seguito al blocco dell’IL-10 endogena indotta da LPS. Al contrario, l’IL-10 endogena non è stata vista avere effetti sulla secrezione di IL-23. Questi risulatati sottolineano l’importanza dell’espressione del GM-CSFR in monociti per la generazione di DC indotta da citochine e guardano al GM-CSF come ad un diretto protagonista nella generazione di DC funzionalmente distinte.
Myeloid dendritic cells (DCs) and macrophages evolve from a common precursor. However, factors controlling monocyte differentiation toward DC or macrophage are poorly defined. We report that surface density of GM-CSF receptor (GM-CSFR) α subunit in human peripheral blood monocytes varies among donors. Although no correlation was found between the extent of GM-CSFR and monocyte differentiation into DC driven by GM-CSF and IL-4, GM-CSFR expression strongly influenced the generation of CD1a+ dendritic-like cells in the absence of IL-4. CD1a+ cells generated in the presence of GM-CSF express CD40, CD80, MHC I and II, DC-SIGN, MR, CCR5, and partially retain CD14 expression. Interestingly, they spontaneously induce the expansion of CD4+ and CD8+ allogeneic T lymphocytes producing IFN-gamma, and migrate toward CCL4 and CCL19. Upon stimulation with TLR ligands, they acquire the phenotypic features of mature DCs. In contrast, the allostimulatory capacity is not further increased upon LPS activation. However, by blocking LPS-induced IL-10, a higher T cell proliferative response and IL-12 production was observed. Interestingly, IL-23 secretion was not affected by endogenous IL-10. These results highlight the importance of GM-CSFR expression in monocytes for cytokine-induced DC generation and point to GM-CSF as a direct player in the generation of functionally distinct DCs.

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16

Mikkelsen, Ipsen Johanna. "Kan onkolytiskt adenovirus armerat med GM-CSF fungera som behandling mot cancer?" Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-43026.

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Cancer är idag en vanlig sjukdom som uppstår på grund av okontrollerad celltillväxt och kan visa sig som cirka 200 olika sjukdomar beroende på vilken celltyp som drabbas. Trots dagens standardterapier med kirurgi, strålning och kemoterapi så dör årligen runt 23 000 människor av cancer i Sverige. Dödsfallen beror ofta på svåråtkomliga metastaser som bildats från ursprungstumören och sedan spridits med blod och lymfa ut i kroppen. En långt gången cancer kan även visa upp resistens mot vissa terapier, vilket försvårar behandling ytterligare. Det är därför viktigt att nya effektiva läkemedel och behandlingsmetoder utvecklas. Ett alternativ är onkolytisk virusterapi. Onkolytiska adenovirus är modifierade till att selektivt replikera i och lysera tumörceller, samtidigt som friska celler lämnas opåverkade. Genom att armera det onkolytiska adenoviruset med cytokinet granulocyt makrofag-kolonistimulerande faktor (GM-CSF) kan den terapeutiska effektiviteten ökas ytterligare. GM-CSF kommer då uttryckas i infekterade tumörceller och stimulera kroppens immunförsvar till ökad antitumoral immunrespons. Syftet med detta arbete var att undersöka om behandling med onkolytiskt adenovirus armerat med GM-CSF kan fungera som behandling mot cancer. För att svara på frågeställningen analyserades fem vetenskapliga studier som rörde frågeställningen. Två av dessa var av fas I-typ och hade därför som främsta syfte att undersöka säkerheten hos olika doser. Den antitumorala effekten studerades dock också och därför inkluderades de i arbetet. Antitumorala effekter sågs hos vissa patienter i form av minskning av tumörstorlek, densitet och tumörmarkörer i blodet. I studier där CD8+ T-celler mättes sågs ofta en ökning av nivån vilket kan tyda på ökad immunrespons. Patientgrupperna var små i samtliga studier vilket gör det svårt att dra några slutsatser om behandlingens effektivitet. I tre av fem studier hade patienterna även olika cancersjukdomar, vilket försvårar analysen ytterligare. Resultaten från behandlingen ser lovande ut med milda biverkningar, men för att med säkerhet kunna säga att det finns en antitumoral effektivitet hos onkolytiskt adenovirus armerat med GM-CSF krävs större studier på mer specifika patientgrupper.

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17

Ladds, Simon John. "The upregulation of neutrophil protein biosynthesis in response to GM-CSF stimulation". Thesis, University of Liverpool, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366718.

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18

Razanajaona, Diane. "Régulation de l'expression génique du GM-CSF dans les cellules hématopoiétiques humaines". Aix-Marseille 2, 1992. http://www.theses.fr/1992AIX22022.

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Le gm-csf est une glycoproteine de la famille des csf (colony-stimulating factor), jouant un role crucial dans la croissance et la differenciation hematopoietique. Son messager appartient au groupe des messagers instables, et son expression est inductible dans les cellules hematopoietiques normales, mais constitutive dans certaines cellules tumorales, telles que les cellules de leucemies aigues myeloides (lam). L'etude de la relation entre ce facteur et les lam montre que son expression est constitutive dans ces cellules, que ce facteur est implique dans leur proliferation autocrine in vitro, et qu'il est capable d'induire ou d'amplifier la proliferation de ces memes cellules. L'etude de la regulation de l'expression genique du gm-csf dans une lignee humaine lymphocytaire t, jurkat, montre une regulation differentielle en fonction du stade d'activation, avec d'abord une stabilisation post-transcriptionnelle, puis une activation transcriptionnelle predominante. Des chasses a l'actinomycine d montrent une variation de la stabilite du transcrit en fonction du temps. L'utilisation de la cycloheximide souligne l'importance des proteines regulatrices dans les mecanismes de regulation des messagers cytoplasmiques

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19

Rothchild, Alissa Chen. "Antimicrobial Roles for iNKT Cells and GM-CSF in Mycobacterium Tuberculosis Infection". Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11371.

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Despite effective antibiotics, Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, still infects nearly one-third of the world's population. While key immune factors including CD4+ T cells and IFNg production have been identified, there are still many antimicrobial mechanisms yet to be explored. Here we characterized the role of invariant natural killer T (iNKT) cells and GM-CSF during Mtb infection.

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20

Goyal, Girija. "Novel Role of PPAR-Gamma in GM-CSF Induced Anti-Tumor Immunity". Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:14226102.

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Granulocyte macrophage colony stimulating factor (GM-CSF) mediates context dependent anti- or pro-inflammatory functions through cells of the myeloid lineage. GM-CSF signaling induces the expression of the transcription factor peroxisome proliferator-activated receptor gamma (PPAR-γ). We examined the role PPAR-γ in myeloid cells in the anti-tumor response to GVAX, a GM-CSF based cancer immunotherapy using the B16 model of murine melanoma. We found that selective loss of PPAR-γ in the myeloid lineage using LysM-Cre reduces the efficacy of GVAX which could not be explained by known mechanisms. RNASeq of GVAX draining lymph node identified an increase in regulatory T-cells markers such as FoxP3 and coinhibitory receptors CTLA-4 and TIGIT in LysM-Cre; PPAR-γ fl mice (PPAR-γ KO). We confirmed by flow cytometry that Treg frequency was indeed increased in PPAR-γ KO lymph node with a strong reduction seen in the ratio of CD8 T-cells to regulatory T cell (CD8:Treg). Treg recruiting chemokines CCL17 and CCL22 were upregulated in the draining lymph node. Importantly, tumors in PPAR-γ KO mice had a reduced CD8:Treg ratio explaining the loss in GVAX efficacy. Pharmacological activation or inactivation of PPAR-γ in GM-CSF treated human PBMC showed conservation of the role of PPAR-γ in regulating T-cell numbers in humans. PPAR-γ agonism in mice, using the FDA-approved small molecule ligand rosiglitazone (Rosi), improved CD8:Treg ratios in the vaccine draining lymph node and tumors. The gain-of-function data suggested the Rosi could be used as an adjunct to immunotherapy. All intratumoral Treg expressed high levels of CTLA-4 and TIGIT. Thus, we tested the impact of Rosi on the response to GVAX and anti-CTLA-4 combination therapy. We found that Rosi improved the tumor incidence and overall survival of tumor bearing mice treated with GVAX and anti-CTLA4. Our data have identified a novel role of PPAR-γ in myeloid cells in regulating Treg numbers. This pathway is conserved in humans as seen in ex-vivo studies of PBMC. Further, we provide preclinical evidence that Rosi can be used to improve immunotherapeutic responses by increasing the ratio between intratumoral effector and regulatory cells.

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21

Kühnle, Simone. "The reconstitution of immunocompetence by GM-CSF or IFN after pharmacological suppression". [S.l. : s.n.], 2001. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB9073784.

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22

Sylvain-Prévost, Stéphanie. "Implication de TAK1 dans la modulation des réponses du neutrophile humain au fMLP et au GM-CSF". Mémoire, Université de Sherbrooke, 2012. http://hdl.handle.net/11143/6362.

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Les neutrophiles sont d'une grande importance dans la première ligne de défense de l'organisme contre les pathogènes. Ils participent activement par leurs actions antimicrobiennes, comme la phagocytose et la relâche de granules, mais influencent également la réponse immunitaire par les différentes cytokines et chimiokines qu'ils produisent. L'étude des différentes fonctions du neutrophile a permis d'établir les étapes clés de la signalisation intracellulaire qui mène à ces différentes fonctions. De plus, les études dé signalisation, dans différents organismes, ont placé TAK1, une MAP3K, à l'avant-plan dans l'activation des sentiers MAP kinase et des facteurs de transcription NF-kB. Nos efforts pour élucider les sentiers métaboliques du neutrophile nous ont fait nous pencher sur le rôle que TAK1 pouvait y jouer. Nous avons donc découvert que TAK1 était la kinase d'importance dans le contrôle des fonctions du neutrophile avec le LPS et le TNF[alpha], deux stimuli activateurs de NF-kB. Dans cette étude, nous nous sommes penchés sur le rôle de TAK1 chez le neutrophile avec des stimuli dont les réponses cellulaires ne passent pas par l'activation de NF-kB. C'est dans cette perspective que nous avons utilisé un chimioattractant, le fMLP, et un facteur de croissance, le GM-CSF. Ce sont deux stimuli physiologiques fréquemment retrouvés aux sites inflammatoires. Le fMLP et le GM-CSF activent rapidement TAK1 et celle-ci se retrouve en amont de la voie MEK/ERK, mais pas des voies p38 MAPK et PI3K/AKT. L'inhibition de TAK1 diminue l'expression et la sécrétion d'IL-8 et d'IL-1RA. L'inhibition de MEK/ERK et de PI3K/AKT a le même effet. De plus, l'inhibition de TAK1 empêche l'effet antiapoptotique du GM-CSF ainsi que diminue la production de leucotriènes par le fMLP. En conclusion, les travaux présentés montrent que TAK1 est une MAP3K essentielle dans les réponses fonctionnelles du neutrophile au fMLP et au GM-CSF. Cette découverte ouvre la porte à de nouvelles cibles thérapeutiques, particulièrement dans le cas de maladies chroniques impliquant le GM-CSF.

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23

Jasper, Melinda Jane. "Paracrine regulation of ovarian function by granulocyte-macrophage colony-stimulating factor (GM-CSF) & colony-stimulating factor-1 (CSF-1) /". Title page and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phj39.pdf.

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24

Xu, Jian. "Selective reconstitution by GM-CSF of the immune response in human immunosuppressed cells". Konstanz, 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965669238.

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25

Hellebrand, Eva. "Entwicklung von GM-CSF-produzierenden EBV-Vektoren für die Immuntherapie der B-CLL". Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-12575.

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26

Cowling, Randy T. "Effect of GM-CSF on RNA and protein in human peripheral blood granulocytes". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ36768.pdf.

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27

Arcanjo, Katia Denise de Souza. "Organização molecular do espaço intercelular na sinalização do GM-CSF em sistemas hematopoeticos". [s.n.], 2002. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317887.

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Orientador : Radovan Borojevic
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-01T08:59:37Z (GMT). No. of bitstreams: 1 Arcanjo_KatiaDenisedeSouza_D.pdf: 8227428 bytes, checksum: ce60d7dcab3f2fe523a6be9c914002b6 (MD5) Previous issue date: 2002
Resumo: O microambiente da medula óssea desempenha importância fundamental na proliferação e diferenciação das células progenitoras hematopoéticas bem como no controle do egresso dessas células para o sangue periférico. Embora moléculas da matriz extracelular, juntamente com citocinas, sejam cruciais na compartimentalização dos microambientes da medula óssea, ainda não se conhecem os pré-requesitos para que um determinado estroma possa sustentar a hematopoese. Usando uma linhagem celular (FDC-Pl) dependente de fator de crescimento, comparamos modelos experimentais de estromas periféricos e de medula óssea, que sustentam ou não a proliferação mielóide "in vitro". Observamos que todos os estromas produzem um grupo similar de hemopoetinas, incluindo o fator estimulador de colônias de macrófagos e granulócitos (GM-CSF), o qual pode ser liberado das monocamadas estromais, através de altas concentrações de sais, numa forma biologicamente ativa. Por outro lado, glicosaminoglicanos (GAGs) obtidos a partir desses estromas, exibiram uma capacidade de modulação da atividade biológica do GM-CSF variável, dependendo da concentração utilizada. Fibroblastos de pele, que não são capazes de sustentar a mielopoese "in vitro", sintetizam GAGs que podem inibir a atividade mielopoética de GM-CSF. Concluímos que, a qualidade dos glicoconjugados pericelulares dos estromas, presentes no microambiente local, é determinante para que um dado estroma seja capaz de sustentar a mielopoese, mesmo quando hemopoetinas biologicamente ativas são localmente produzidas. Os aspectos espaciais desse microambiente e as interações moleculares entre as células do estroma e progenitores mielóides foram investigados. Demonstramos que esse contato fisico pode disparar um "capping" de moléculas de superfície celular incluindo glicoconjugados de ácido siálico e proteoglicanos. Juntas, essas moléculas, potencialmente interativas com o GMCSF, geram um ambiente intercelular esfecífico, promovendo condições fisico-químicas requeri das para essa interação. A identificação da expressão dos HSPGs associados as superfícies celulares foi monitorada através de RT -PCR. Os estromas analisados mostraram expressão de mRNA para glipicam, betaglicam e sindecam-4. O tratamento das monocamadas estromais com PI-PLC (fosfolipase C) e tripsina branda, confinnou a presença de HSPGs de superfície celular (glipicam) e sindecam, respectivamente. Aproximadamente, 20% dos HSPGs obtidos, estão associados à membrana através de âncoras de GPI enquanto o restante, 80%, permanece integrado à membrana plasmática. Demonstramos que as moléculas marcadas com sulfato radioativo, deslocadas da superfície celular das células estromais após tratamento com tripsina branda, são capazes de aumentar a atividade biológica do GM-CSF, quando comparadas com aquelas deslocadas por PIPLC as quais não apresentaram diferenças significativas se comparadas com o controle. Esses resultados sugerem a existência de HSPGs transmembranares e associados via âncora de GPI nas superfícies das células estromais, e que, a atividade biológica de GM-CSF na proliferação de FDC-Pl "in vitro", é aumentada através de uma possível interação física entre o fator de crescimento e um HSPG transmembranar
Abstract: The bone marrow microenvironrnent plays an important role in promoting hematopoietic progenitor cell proliferation and differentiation, as well as their controlled release into the circulation. It has been shown that the extracellular matrix elements in combination with cytokines are crucial for compartmentalization of the bone marrow environrnent, but it is not clear which are the molecular and structural requirements for a given stroma to sustain hematopoiesis. Using the growth factor-dependent cell line FDC-Pl, we have compared in vitro experimental models of bone marrow and peripheral stromas, two of which sustain myeloid proliferation and one which does not. We have found that all the stromas produced a similar set of hemopoietins, including the GM-CSF, which could be released from the stromal cell layer in an active form by high-salt buffers. On the other hand, glycosaminoglycans (GAGs) obtained from stromas had variable concentration-dependent capacity to modulate the GM-CSF activity. The skin fibroblasts, which can not sustain myelopoieis in vitro, synthesized GAGs that could inhibit the myelopoiesis-promoting activity of GM-CSF produced by the same cells. We conclude that the quality of the stroma pericellular glycoconjugates, present in microenvironrnent, is determinant for the ability of a given stroma to sustain myelopoiesis, even when biologically active hemopoietins are locally produced. The spatial organization of this microenvironrnent and molecular interactions among stroma cells and myeloid progenitors was investigated, and we have shown that the physical intercellular contact triggers the capping of cell surface molecules, including sialylated glycoconjugates and proteoglycans. Together, they generated the specific intercellular environrnent, rich in molecules potentially interactive with GM-CSF, and providing the physicochemical conditions required for this interaction. We have partially assessed the identification of the core proteins of cell-associated HSPGs of the stromal cell lines monitoring their expression by RT-PCR. The assayed stromas expressed mRNA for glypican, syndecan-4 and betaglycan. The stromal layers treatment with PI-PLC and mild trypsin confirmed the presence of hydrophobic cell surface HSPG glypican and syndecan, respectively. About 20% of the HSPG are linked to membrane by glycosilphosphatidylinositol (GPI) anchor while the remainder, 80%, are integrated in the plasma membrane. We have shown that the 35 -s labeled molecules dislodged from stroma cell membranes by mild treatment with trypsin increased the biological activity of the GM-CSF, whilst those dislodged by phospholipase-C did noto These results suggested the existence of both transmembrane HSPG and GPI-HSPG and that the biological activity of GM-CSF in FDC-Pl proliferation, in vitro, is increased by a physical interaction between growth factor and transmembranar HSPG
Doutorado
Biologia Celular
Doutor em Biologia Celular e Estrutural

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28

Stomski, Frank Charles. "The molecular basis of IL-3, Il-5 and GM-CSF receptor activation /". Title page, contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phs8766.pdf.

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29

Pfeiffer, Hella [Verfasser], e Walburga [Akademischer Betreuer] Dieterich. "Bestimmung der Oberflächenmarker und des Aktivierungsgrades von CD14+ Zellen aus humanem Blut nach Stimulation und Reifung mit IL-4/GM-CSF oder IL-15/GM-CSF / Hella Pfeiffer. Gutachter: Walburga Dieterich". Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2015. http://d-nb.info/1075838045/34.

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30

Baker, David Alan. "Mutational analysis of the proto-oncogenes c-fms and c-kit". Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362390.

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31

Curé, Hervé. "Intensification de la chimiotherapie neo-adjuvante du cancer du sein : impact sur la reponse et la survie et etude des cellules souches hematopoietiques peripheriques (doctorat : hemato-cancerologie)". Clermont-Ferrand 1, 1999. http://www.theses.fr/1999CLF1MM15.

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32

DE, GENTILE ALBANE. "Etude de l'expression et de la modulation par l'acide retinoique des recepteurs du gm-csf et de cytokines dans les leucemies aigues promyelocytaires. Production d'anticorps diriges contre le recepteur du gm-csf". Paris 6, 1994. http://www.theses.fr/1994PA066580.

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Ce travail comporte deux parties. Dans un premier temps, nous presentons les resultats de l'etude in vitro: 1) de l'expression des recepteurs du gm-csf (r-gm-csf) par les cellules leucemiques de patients atteints de leucemie aigue promyelocytaire. (lam 3) ; 2) de la production de cytokines par ces memes cellules leucemiques ; 3) de la modulation de cette production ainsi que de l'expression des recepteurs au cours de la differenciation granulocytaire induite par l'acide retinoique tout trans (atra). Nos travaux montrent que les cellules de lam 3 expriment les recepteurs du gm-csf et que cette expression est modulee au cours de la differenciation par l'atra. Les changements (augmentation du nombre et/ou de l'affinite des recepteurs) sont correles a l'efficacite de differenciation induites par l'atra mais pas a la croissance cellulaire. Les cellules de lam 3 expriment et secretent des cytokines. Le profil d'expression des cytokines par les lam 3 est fortement relie a la reponse des cellules a l'atra. De plus, l'atra peut parfois entrainer une modulation de la production de cytokines. Cette modulation est correlee a une augmentation du nombre de cellules leucemiques. Ces resultats nous ont permis de montrer que in vitro le r-gm-csf n'etait pas implique dans l'augmentation du nombre de cellules et que les cytokines ont un role important dans la reponse des lam3 a l'atra ainsi que dans la proliferation cellulaire associee a cette pathologie. Dans un second temps, nous avons produit des anticorps diriges contre le r-gm-csf. De tels anticorps n'avaient pas encore ete decrits lorsque nous avons commence ce travail. Nous avons donc produit une proteine de fusion comportant un fragment du r-gm-csf associe a la proteine mbp (maltose binding protein). Nos resultats montrent la strategie et la methodologie que nous avons employees pour obtenir 3 anticorps monoclonaux

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33

Szymanski, Silvia. "Evaluation of different approaches to enhancing arteriogenesis using isolated monocytes and GM-CSF treatment in an ischemic mouse hind limb model". Giessen : VVB Laufersweiler, 2006. http://geb.uni-giessen.de/geb/volltexte/2007/4335/index.html.

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34

Feil, Bertram. "Genexpression des Adaptorproteins Shc bei Patienten mit Juveniler Myelomonozytärer Leukämie (JMML) Charakterisierung neuer Spleißformen der SH2-Domäne von Shc /". [S.l. : s.n.], 2000. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB8937685.

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35

Houzet, Laurent. "Etude du rôle des séquences AU riches de l'ARNm du GM-CSF in vivo". Doctoral thesis, Universite Libre de Bruxelles, 2001. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211667.

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36

LICARI, VERONIQUE. "Maladie de kaposi localisee chez un sujet hiv negatif : action antitumorale du gm-csf". Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20131.

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37

Kühnle, Simone. "The reconstitution of immunocompetence by GM-CSF or (IFN-g) [(IFN-gamma)] after pharmacological suppression". [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=961227540.

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38

Harris, Robert John. "Studies of the production and function of GM-CSF in LTBMC and mature B cells". Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266492.

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39

Fernandez, Marilyn Cecilia. "Mechanisms regulating GM-CSF and TNF-alpha induced IL-1(beta) gene expression in PMN /". The Ohio State University, 1997. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487942739808581.

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40

Deane, David Leslie. "The characterisation of a GM-CSF and IL-2 inhibitory protein encoded by Orf virus". Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/23323.

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In this study, the gene encoding the GM-CSF inhibitory factor (GIF) was isolated and mapped to the right terminal quarter of the orf virus genome. The orf virus GIF cDNA was expressed as a secreted protein in Chinese hamster ovarian cells as detected by GM-CSF inhibition ELISA. Recombinant GIF was purified by ovine GM-CSF affinity chromatography and gel filtration. Sequence analysis of the 20 N-terminal amino acids was performed on the purified GIF. The GIF gene encodes a 28 kDa protein that exhibits 32% amino acid sequence similarity to the predicted sequence of the A41L gene product encoded by vaccinia virus. Although the vaccinia virus A41L protein has sequence similarity to the T1 secreted chemokine-binding proteins of leporipoxviruses, its function is not known. GIF did not share any homology with any cytokine receptor molecule identified to date. In contrast to other parapoxvirus immunomodulatory proteins that are products of early viral genes, GIF was found to be the product of an intermediate/late viral gene of orf virus infected cells. GIF formed homodimers and homotetramers in solution and bound ovine GM-GSF with a Kd of 369 pM. In addition GIF bound ovine IL-2 with a Kd of 1.04 nM. Although orf virus infects humans, GIF did not bind human GM-CSF or IL-2. GIF was shown to inhibit the binding of ovine GM-CSF labelled with ¹²⁵I to its receptor on isolated sheep neutrophils and it inhibits the haematopoietic activity of ovine GM-CSF in a soft agar bone marrow colony assay. GIF also inhibited the binding of ovine IL-2 labelled with ¹²⁵I to CD4⁺ T cells and inhibited the stimulatory activity of ovine IL-2 in a T cell proliferation assay. This inhibitory activity was neutralised by a rabbit antiserum raised against purified GIF. GIF was produced in vivo during orf virus reinfection. GIF was detected in skin, localised to the area of orf virus infected cells and in afferent lymph draining the skin site of infection. The presence of GIF, 3-7 days after virus infection was associated with reduced levels of GM-CSF in the lymph plasma and the period of maximum viral replication in the skin.

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41

Paolini, Léa. "Impact de l’acide lactique sur le phénotype et le métabolisme des macrophages humains". Thesis, Angers, 2018. http://www.theses.fr/2018ANGE0036.

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Les macrophages associés aux tumeurs (TAM) orchestrent l'inflammation nécessaire à la croissance tumorale (propriétés de type M1) et favorisent les métastases et l'angiogenèse (caractéristiques de type M2). Cependant, la nature des facteurs capables de conférer des propriétés M1 et M2 aux macrophages humains demeure inconnue. L'acide lactique (AL) est un métabolite produit par les cellules tumorales connu pour moduler les fonctions des cellules présentes dans le microenvironnement tumoral. Dans cette étude, nous avons analysé son impact sur la différenciation des monocytes humains. Les résultats montrent que l’AL induit la différentiation des monocytes (cultivées en présence de GM-CSF) en macrophages présentant un phénotype atypique (CD14high CD163high IL-10low IL-12low) et, de manière intéressante, des caractéristiques phénotypiques M1 (production de cytokines inflammatoires) et M2 (production de facteurs de croissance, expression de gènes prototypiques M2). Un profil similaire est obtenu lorsque les monocytes sont cultivés avec des cellules cancéreuses primaires glycolytiques. Ces effets de l'AL sur la polarisation des macrophages nécessitent l'entrée du lactate dans les cellules (via le transporteur MCT-1) et son oxydation en pyruvate et sont médiés par une stabilisation de HIF-1α et une consommation autocrine de M-CSF.Ces résultats (i) identifient l'AL comme un médiateur induisant la génération de macrophages humains présentant des caractéristiques M2 et des propriétés inflammatoires et (ii) renforcent l'intérêt de l’utilisation des inhibiteurs de la glycolyse aérobie pour moduler les fonctions des TAM
In established tumors, tumor-associated macrophages (TAM) orchestrate unresolving cancer-related inflammation (M1-related properties) and favor tumor development, metastasis and angiogenesis (M2-like properties). However, to date, the nature of the polarization factor(s) able to confer M1 and M2 functional properties to human macrophages remains unknown.Lactic acid (LA), a metabolite produced at high levels in most established tumors, can impact the phenotype and functions of cells present in the tumor microenvironment. In this study, we analyzed the impact of LA on the human monocyte differentiation. Results showed that LA skews monocytes (differentiated in the presence of GM-CSF) into macrophages (GM+LA-Mφ) exhibiting an atypical CD14high CD163high IL-10low IL-12low phenotype. Interestingly they harbor M1 and M2 phenotypic features, as assessed the production of a wide variety of inflammatory and growth factors and the expression of prototypic M2-like genes. A similar profile is induced by culturing monocytes with glycolytic human primary cancer cells. These effects of LA on macrophage polarization require the entry of lactate into the cells (via the monocarboxylate transporter 1) and its oxidation into pyruvate and are mediated via HIF-1α stabilization and autocrine M-CSF consumption by differentiating cells. These results identify tumor-derived LA as a missing link reconciling the M2-like features of TAM with their inflammatory properties. They also reinforce the interest of aerobic glycolysis inhibitors to modulate the functions of TAM

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42

Robertson, Sarah A. "Granulocyte-macrophage colony stimulating factor (GM-CSF) : a paracrine regulator in the pre-implantation mouse uterus". Title page, abstract and contents only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phr6515.pdf.

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43

Rajotte, Daniel. "Étude sur la signalisation intracellulaire et la relation structure fonction du récepteur pour le GM-CSF". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21506.pdf.

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Kidger, Simone Verina. "The impact of the synovial environment and GM-CSF on the myeloid compartment in rheumatoid arthritis". Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8012/.

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The synovial environment in rheumatoid arthritis (RA) is a milieu of Damage Associated Molecular Patterns (DAMPs), cytokines and immune complexes, which can modulate the activation or polarisation of myeloid cells. GM-CSF, which is a pivotal myeloid cell growth factor, is also a pro-inflammatory cytokine that drives aspects of RA immunopathogenesis. Inhibition of GM-CSF signalling has been successful in both mouse models and in clinical trials for RA, however, the specific effect of GM-CSF on myeloid cells in a synovial setting is not well understood. The aim of this thesis was to investigate the impact of the synovial environment and GM-CSF on myeloid cells in RA. GM-CSF stimulation induced monocytes to secrete substantial amounts of the chemokine CCL17. However, this induction of CCL17 was significantly inhibitedupon co-stimulation with RA synovial fluid, but not osteoarthritis (OA) synovial fluid, whilst the expression of other chemokines was unaffected. TLR ligands also inhibited GM-CSF driven CCL17, however, through the use of MyD88/TRIF knockout mouse monocytes, we found RA synovial fluid inhibition of CCL17 was TLR-independent. Small Immune Complexes and IFNα also had the capacity to inhibit GM-CSF induction of CCL17, suggesting multiple mechanisms within the RA synovial fluid to prevent this induction. Despite the consistency of RA synovial fluid causing inhibition of the GM-CSF signalling pathway in comparison to OA synovial fluid, there were no distinct effects on macrophage polarisation. The RA synovial environment has more of an impact on monocyte activation in comparison to macrophage polarisation, as synovial fluid from other arthropathies had the comparable effects on macrophage phenotypes. This thesis concludes that RA synovial fluid contains several factors that inhibit GM-CSF induction of CCL17. This suggests a regulatory mechanism, preventing the excessive secretion of CCL17 by monocytes, thereby preventing exacerbation of immunopathogenesis.

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Nataf, Éric. "Etude cytogenetique du myelome multiple : a propos de 49 patients ; interet de l'utilisation gm. - csf - il6 - il3". Lille 2, 1992. http://www.theses.fr/1992LIL2M180.

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46

OLAGNIER, VALERIE. "Essai multicentrique en double aveugle ou cho-cell-gm-csf dans les neuroblastomes de haut grade traites par double autogreffe medullaire". Lyon 1, 1989. http://www.theses.fr/1989LYO1M323.

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47

Weininger, Eva-Maria [Verfasser], Juan Manuel [Akademischer Betreuer] Maler, Jun Manuel [Gutachter] Maler e Philipp [Gutachter] Spitzer. "GM-CSF und M-CSF in Serum und Liquor bei der Alzheimer-Erkrankung / Eva-Maria Weininger ; Gutachter: Jun Manuel Maler, Philipp Spitzer ; Betreuer: Juan Manuel Maler". Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2020. http://d-nb.info/1203377649/34.

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48

Hüttinger, Cornelia. "Nonviraler Gentransfer des felinen Zytokin-Gens GM-CSF mittels Magnetofektion als neoadjuvante Immuntherapie beim Fibrosarkom der Katze". Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-89747.

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49

Walsch, Florian Markus. "Nonviraler Gentransfer des felinen Zytokin-Gens GM-CSF mittels Magnetofektion als neoadjuvante Immuntherapie beim Fibrosarkom der Katze". Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-147715.

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50

CREISSON, DUCRAY ANNE. "Lymphomes non-hodgkiniens agressifs du sujet age : resultat du protocole memid avec et sans rh-gm-csf". Nice, 1993. http://www.theses.fr/1993NICE6536.

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Tesi sul tema "GM-CSF"

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