Rozprawy doktorskie na temat „Macrophage”
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Svensson, Ulf. "Macrophage activation by bacteria signalling to prostaglandin and cytokine responses /". Lund : Dept. of Medical & Physiological Chemistry, Lund University, 1994. http://books.google.com/books?id=sAhrAAAAMAAJ.
Pełny tekst źródłaHiguera, González Laura 1993. "Novel transcription regulators of tissue macrophages and alternative macrophage polarization". Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2021. http://hdl.handle.net/10803/672702.
Pełny tekst źródłaLos macrófagos juegan un papel muy importante en la defensa del organismo frente a una amplia variedad de patógenos. Los macrófagos se adaptan rápidamente a las perturbaciones en el microambiente gracias a que existe una compleja red de factores de transcripción que modulan sus respuestas. En los últimos años se han identificado factores de transcripción que regulan la identidad de los macrófagos, sin embargo, apenas se está comenzando a conocer la importancia de otros factores de transcripción que permiten adaptar la respuesta de los macrófagos, tanto en condiciones homeostáticas como frente a infecciones. Anteriormente nuestro grupo identificó reguladores transcripcionales de las respuestas pro-inflamatorias de los macrófagos, y en este trabajo hemos explorado la función de nuevos mecanismos reguladores que participan en la regulación de la distribución de los macrófagos en homeostasis, así como en las respuestas anti-inflamatorias de los macrófagos. Hemos estudiado poblaciones de macrófagos con diferentes ontogenias que habitan dentro de los tejidos y hemos caracterizado su regulación transcripcional. Además, hemos comparado la respuesta anti-inflamatoria de los diferentes macrófagos tisulares y así hemos identificado que existe un mecanismo transcripcional específico que controla la expresión de genes anti-inflamatorios según el origen del macrófago.
Tabata, Yasuhiko. "Macrophage phagocytosis of polymer microspheres and antitumor activation of macrophages". Kyoto University, 1987. http://hdl.handle.net/2433/74704.
Pełny tekst źródłaRaborn, Erinn Shenee. "Cannabinoid Modulation of Chemotaxis of Macrophages and Macrophage-like Cells". VCU Scholars Compass, 2007. http://hdl.handle.net/10156/1333.
Pełny tekst źródłaAdler, Heiko. "Fetal bovine bone marrow-derived macrophages : a model for studying basic aspects of macrophage biology and pathogen-macrophage interaction in cattle /". [S.l.] : [s.n.], 1994. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
Pełny tekst źródłaGrand-Perret, Thierry A. R. "Induction d'une activité anti-tumorale chez les macrophages péritonéaux murins". Paris 11, 1986. http://www.theses.fr/1986PA112301.
Pełny tekst źródłaDi, Maggio Paula. "Dietary lipids and inflammation : chylomicron remnants suppress pro-inflammatory pathways and activate antioxidant defence mechanisms in human macrophages". Thesis, Royal Veterinary College (University of London), 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618287.
Pełny tekst źródłaSoe-Lin, Shan. "Macrophage iron recycling". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66717.
Pełny tekst źródłaLa majorité du fer dans le corps humain est contenu dans la masse de globule rouge, en tant que composante de l'hémoglobine. Les GR deviennent plus endommagés et moins déformables en vieillissant, et à la fin de leurs durée de vie de 120 jours, les GR sénescents sont ingurgités par les macrophages du système réticuloendothélial du foie et de rate. Ces macrophages spécialisés ingèrent 2 millions de GR∕sec, catabolisent l'hémoglobine et relâche le fer qui y est contenu à la transferrine plasmatique pour permettre son réincorporation dans de nouveau GR dans la moelle épinière. C'est remarquable comment les macrophages réticuloendothéliaux gèrent de manière sécuritaire l'énorme quantité de fer qui serait sinon toxique pour les autres cellules. Dans mes recherches, j'ai examiné les aspects spécifiques du métabolisme du fer dans ces macrophages spécialisés dans sa manutention.La protéine associée à la résistance naturelle du macrophage (Nramp1) est un transporteur de métaux divalents exprimé seulement dans les phagosomes de cellules phagocytiques telle que les macrophages et les neutrophiles. Nramp1 a depuis été reconnu comme le gène responsable de conférer à l'hôte la résistance contre les pathogènes intracellulaires. Nramp 1 est présumé donner une protection en vidant le phagosome de métaux divalents nécessaires à la croissance de pathogènes.Au cours des recherches nous avons trouvé qu'en plus de jouer un rôle significatif dans la résistance de l'hôte, Nramp1 est aussi important pour la régularisation de l'homéostasie du fer. Nous avons remarqué que les macrophages sans Nramp1 sont incapables de recycler le fer (après l'erythrophagocytose in vitro) de manière aussi efficace que les macrophages qui ont le Nramp1 fonctionnel. On a ensuite observé les souris knockout et trouvé que les animaux sans Nramp1 ont une surdose progressive de fer en vieil
Georges, George Tharwat. "Novel Characteristics of Murine Bone Marrow-Derived Macrophages and Human Macrophage-Like Cells". VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd/932.
Pełny tekst źródłaSobhani, Kimia. "Proteomic analysis of macrophage proinflammatory programmed cell death and macrophage activation /". Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8688.
Pełny tekst źródłaAwomoyi, Agnes Abiola Oluwatoyin. "Genetics of susceptibility to tuberculosis". Thesis, Open University, 2000. http://oro.open.ac.uk/58012/.
Pełny tekst źródłaDavis, John Beresford. "The macrophage in atherogenesis". Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276341.
Pełny tekst źródłaFalck-Hansen, Mika André. "Macrophage regulation in atherosclerosis". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29863.
Pełny tekst źródłaDewhurst, Jennifer. "Macrophage subpopulations in COPD". Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/macrophage-subpopulations-in-copd(e0e66fa4-ddff-4591-b785-edee74918539).html.
Pełny tekst źródłaDavies, Luke C. "Control of macrophage homeostasis". Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/112185/.
Pełny tekst źródłaBouchareychas, Laura. "Implication des phagocytes mononuclées dans l'évolution de la plaque d'athérosclérose et relation avec l'homéostasie du cholestérol et des lipoprotéines". Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066282/document.
Pełny tekst źródłaAtherosclerosis represents a chronic pathophysiological process implicated in the majority of cardiovascular diseases. The development of atherosclerotic lesions is characterized by an accumulation of extra and intracellular lipids in the arterial wall at the origin of a strong inflammatory response involving macrophages.Macrophages are considered key actors in the development of atherosclerotic plaques. Indeed, because of their ability to metabolize cholesterol (capture, storage, efflux), to regulate inflammation and to phagocyte apoptotic cells, they exert pro and/or anti-atherogenic functions that may be modulated therapeutically. In this context, we evaluated the therapeutic potential of macrophages protected against apoptosis, on the progression of established atherosclerotic lesions.We have demonstrated that increased macrophage survival can slow down the progression of established lesions, stabilize lesion and reduce cholesterol levels. These athero-protective effects are attributed to the increase in Kupffer cells and Ly-6Clow monocytes partly due to their ability to produce apolipoprotein E. We also show that Kupffer cells are involved in the clearance of pro-atherogenic lipoproteins. The increase in ApoE pool and in Kupffer cells reduces cholesterol levels and thus lesion progression
Lisowski, Zofia Maria. "Targeting the macrophage in equine post-operative ileus". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/33191.
Pełny tekst źródłaAlhanghari, Mofeda Abdussalam. "The Anti-Apoptotic Effect of HSV-1 ON Murine Macrophages: RAW 246.7Murine Macrophage Cell Line". Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1472747895.
Pełny tekst źródłaLévêque, Manuella. "Résolution de l'inflammation - infection dans les macrophages de patients atteints de mucoviscidose : impact de la membrane". Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B041/document.
Pełny tekst źródłaMacrophages play a significant role in the initiating stages of immune responses regulating inflammation and clearance of the pathogens. In cystic fibrosis, inability of the macrophage to act as a suppressor cell leading to chronic inflammation/infection cannot be resolved. The aims of this work was to find new targets responsible for alterations in cystic fibrosis macrophages. Regarding inflammation, the soluble form of CD14 (sCD14), find overproduced by cystic fibrosis macrophages, is characterized to be a DAMP as it contributes for maintenance of inflammation in tissues. Regarding infection, the activity of TRPV2, involved in phagocytic capacity of macrophage, is impaired. In cystic fibrosis, inflammation and infection were closely linked to the alteration of the plasma membrane microstructures involved in the production of sCD14 and in the phagocytosis process. In conclusion, the alterations of macrophage weaken innate defense of cystic fibrosis patients and may be involved in cystic fibrosis disease progression and lung damage. Consequently, interventions aimed to reduce ongoing infection and destructive inflammatory response may be beneficial in order to preserve their lung function. In this way, therapeutic approaches aimed to correct cystic fibrosis macrophages dysfunctions might provide improved resolution of infection and inflammation
Foo, Suan Sin. "Deciphering the Role of Macrophage Subsets and Macrophage-Derived Factors During Arthrogenic Alphaviral Infection". Thesis, Griffith University, 2015. http://hdl.handle.net/10072/365249.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Institute for Glycomics
Science, Environment, Engineering and Technology
Full Text
Merlin, Johanna. "Étude de l’influence de la glutaminolyse des macrophages dans les maladies cardio-métaboliques". Electronic Thesis or Diss., Université Côte d'Azur, 2020. http://theses.univ-cotedazur.fr/2020COAZ6016.
Pełny tekst źródłaChronic inflammatory diseases such as obesity or atherosclerosis are a major public health concern in the western countries. It is now well established that immune cells, and in particular macrophages, play a critical role in the initiation and progression of cardiometabolic diseases. Indeed, tissue resident macrophages control tissue homeostasis such as visceral adipose tissue expansion and brown adipose tissue thermogenesis. However, the underlying mechanisms remain unknown. Immuno-metabolism is a new research area that illustrates macrophage adaptability to their nutritional environment for their function maintenance. We therefore looked at the role of glutamine in macrophage homeostasis and its impact on obesity and atherosclerosis. Therefore, we genetically abolished the limiting enzyme hydrolyzing glutamine to glutamate, called glutaminase 1 (Gls1), specifically in myeloid cells.In our first study, our data demonstrate that Gls1 deficiency in myeloid cells leads to glucose intolerance on a high-fat diet. This is associated with a decrease in norepinephrine levels in brown adipose tissue leading to defective thermogenesis. Our results highlight a decrease in spinal cord macrophage adhesion to glutamatergic neurons leading therefore to a decrease in neuron activation. Thus, our study demonstrates the role of macrophage glutaminolysis in controlling the sympathetic tone of thermogenic adipose tissue.Secondly, we studied the impact of myeloid cell glutaminolysis on atherosclerosis development. Glutaminolysis invalidation in myeloid cells leads to an increase atherosclerotic plaque area. In particular, we observed an increase in plaque necrosis suggesting a new function for macrophage glutaminolysis. We also validated this association in human atheromatous plaques. Although Gls1 deficiency in macrophages does not affect their survival, we showed a key role of this pathway in efferocytosis. Further analyses of the downstream mechanisms revealed an alteration in macrophage alternative polarization associated with mitochondrial metabolism reprogramming. Modulation of these pathways leads to a drop in Rac1 activity, thus explaining the efferocytosis defect. Therefore, our second study identifies myeloid cell glutaminolysis as an essential actor in atherosclerosis development
Reichard, Adam Craig. "The Effects of HSV-1 Challenge on Polarized Murine Macrophages: an In Vitro Model Using the J774A.1 Murine Macrophage Cell Line". Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1343411395.
Pełny tekst źródłaKluftinger, Janet Louise. "Macrophage interaction with Pseudomonas aeruginosa". Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29129.
Pełny tekst źródłaScience, Faculty of
Microbiology and Immunology, Department of
Graduate
Truman, Lucy. "Macrophage chemotaxis to apoptotic cells". Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29404.
Pełny tekst źródłaHeasman, Sarah Jane. "Glucocorticoid modulation of macrophage function". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29146.
Pełny tekst źródłaMcMurray, Heather Forbes. "Macrophage growth factors in atherogenesis". Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306460.
Pełny tekst źródłaRossi, B. C. "Macrophage function in African trypanosomiasis". Thesis, Brunel University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.373784.
Pełny tekst źródłaMcCarthy, Sean Patrick. "Studies on human macrophage heterogeneity". Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238184.
Pełny tekst źródłaWright, Adam. "The macrophage in cystic fibrosis". Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/8783.
Pełny tekst źródłaPound, J. D. "Parameters of human macrophage activation". Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381442.
Pełny tekst źródłaReid, Vanessa Claire. "Macrophage toxicity of lipid oxidation". Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308384.
Pełny tekst źródłaSavill, John Stewart. "Macrophage recognition of senescent neutrophils". Thesis, Imperial College London, 1989. http://hdl.handle.net/10044/1/47641.
Pełny tekst źródłaVoelz, Kerstin. "Macrophage – cryptococcus interactions during cryptococcosis". Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/1194/.
Pełny tekst źródłaHegyi, Laszlo. "Macrophage apoptosis and human atherosclerosis". Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627017.
Pełny tekst źródłaCano, Antonella. "Characterization of Acanthamoeba macrophage activation". Thesis, University of Strathclyde, 2015. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=25992.
Pełny tekst źródłaGoding, Linda M. "Macrophage Recognition of Xenogeneic Erythrocytes". University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1197469419.
Pełny tekst źródłaErwig, Lars-Peter. "Macrophage programming in inflammatory disease". Thesis, University of Aberdeen, 2004. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU194083.
Pełny tekst źródłaHunter, Catriona Mhairi. "MicroRNA regulation of macrophage activation". Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/31027.
Pełny tekst źródłaHolmes, Benjamin A. "The Construction of a Plasmid for Detecting the Pathway of Arginine Metabolism in Human Macrophages: a Real-Time Assessment of Macrophage Polarity". Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1348874681.
Pełny tekst źródłaShabo, Ivan. "Macrophage antigen expression in breast and colorectal cancers : A consequence of macrophage - tumour cell fusion?" Doctoral thesis, Linköpings universitet, Kirurgi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-54820.
Pełny tekst źródłaPark, Young Mi. "Interaction between CD36 and Oxidized LDL Modulates Macrophage Cytoskeletal Functions: A Mechanism of Macrophage Trapping". Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270624670.
Pełny tekst źródłaEllouze, Mehdi. "Identification des mécanismes anti-inflammatoires de GILZ dans les monocytes/macrophages et de son potentiel thérapeutique dans le choc septique". Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS239/document.
Pełny tekst źródłaSepsis and septic shock, associated with a severe and uncontrolled systemic inflammation, are the main causes of death in intensive care units. Macrophages play a central role in these pathologies. They are involved in the initiation and regulation of inflammation. They recognize LPS from the bacterial cell wall via TLR4, which triggers the activation of MAPK signaling pathway and transcription factors such as NF-KB and AP1 and ultimately, the production of pro-inflammatory cytokines including TNF and IL6. The expression of the protein GILZ in macrophages limits in vitro the production of IL6 and TNF in response to LPS. This effect is attributed to inactivation of NF-kB. Moreover, GILZ expression decreases in human and mouse macrophages exposed to LPS.Given the regulatory effects of GILZ in macrophages, the objectives of our study were 1) to determine whether GILZ expression is down-regulated in monocytes / macrophages (M/M) in the sepsis, 2) to determine whether the modulation of GILZ expression in M/M is sufficient to influence systemic inflammation, and 3) to identify GILZ mechanism of action in human M/M.GILZ expression was measured in the M/M of patients with septic shock or acute respiratory distress syndrome, and in a murine model of endotoxemia. We observed a significant reduced expression of GILZ in these pathological contexts in human and mice. The impact of this alteration was explored in unique transgenic mouse model in which macrophages stably overexpress GILZ (CD68-GILZ).We confirmed that GILZ overexpression limits TNF production and promotes IL-10 production in in vitro LPS-stimulated macrophages. We further studied the inflammatory response and survival of these mice in models of endotoxemia and septic shock. We showed that GILZ overexpression restricted to macrophages, limits serum pro-inflammatory cytokines production, therefore decreases systemic inflammation and significantly improves mice survival. These results highlight the effects of macrophage polarization by GILZ at a systemic level.This result confirmed the need to characterize GILZ interactome in human macrophages. Two complementary approaches have been used. The first one consists of a pan-genomic double hybrid screening of human GILZ partners. The second method consists of a tandem affinity purification (TAP-TAG) of GILZ protein and its associated partners, followed by the identification of these partners by mass spectrometry. Analyses have been performed independently on nuclear and cytoplasmic extracts from human macrophage cells, genetically engineered to express GILZ protein with the two tags required for purification. This dual approach led us to identify new direct and indirect interactions between GILZ and other key proteins of TLR4 signaling pathway in human macrophages and highlight a likely role of GILZ as a transcription regulatory factor.These results confirm the anti-inflammatory role of GILZ on systemic inflammation and enhancement of lifetime in murine models of endotoxemia and septic shock. Furthermore, this work identifies for the first time the cytoplasmic and nuclear GILZ partners in human macrophages and would allow in the future, a better understanding of GILZ mechanism of action
Delfini, Marcello. "Jun regulates monocyte-derived macrophage accumulation and tumour progression". Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0076.
Pełny tekst źródłaMacrophages are immune cells present in every organ. Given their variety of functions, macrophages are therapeutic targets in many diseases including cancer. Despite the research efforts to characterise their origins, the molecular mechanisms regulating macrophage differentiation are still poorly defined. Expression of the AP-1 factor, Jun, increases during differentiation, but its role in macrophage development is not known.During my PhD, we characterised how Jun affects macrophage development and homeostasis. We developed a conditional mouse model in which Jun is deficient in the myeloid lineage (JunΔCsf1r). We showed that Jun controls CSF1-mediated monocyte to macrophage differentiation, proliferation and survival. In vivo, Jun loss limits macrophage accumulation in lungs and intestine. Tumour-associated macrophages (TAMs) play critical roles in cancer progression. We observed that Jun deficiency dampens melanoma growth and the differentiation of CSF1-dependent monocyte-derived TAMs. We further showed that Jun-dependent TAMs mediate vessel normalisation in melanoma. During inflammation, Jun was dispensable for the recruitment of monocyte-derived inflammatory macrophages.Altogether, our results identify Jun as a master regulator of macrophage differentiation, without altering monocyte effector functions. In a melanoma model, we showed that Jun-dependent TAMs play tumour-promoting roles. Therefore, Jun is a selective regulator of CSF-1-dependent macrophage development, which is redundant during inflammation; this observation should help to define novel approaches to selectively target macrophage differentiation, without altering monocyte-dependent immune responses
Chanez, Pascal. "Hétérogéneité morphologique et fonctionnelle des macrophages des voies aériennes de l'asthmatique". Montpellier 1, 1994. http://www.theses.fr/1994MON1T038.
Pełny tekst źródłaRivier, Agnès. "Activation des phagocytes mononucléés chez les sujets normaux et les sujets asthmatiques/ Agnès Rivier". Montpellier 1, 1994. http://www.theses.fr/1994MON1T020.
Pełny tekst źródłaHaddad, Elias K. "Study of the role of macrophage activation and macrophage derived cytotoxic factors in early embryo loss". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ29928.pdf.
Pełny tekst źródłaHaddad, Elias K. "Study of the role of macrophage activation and macrophage derived cytoxic factors in early embryo loss". Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42023.
Pełny tekst źródłaIt is known that interferon-$ gamma$ (IFN-$ gamma$) is the major cytokine responsible for the priming of macrophages and that LPS can trigger primed macrophages to produce nitric oxide. Therefore, the observation that exogenous LPS induced embryo abortion in most strains of pregnant mice suggested that the decidual macrophages have been previously primed in situ. To investigate the role of IFN-$ gamma$ as a potential priming signal for decidual macrophage activation, we studied the effect of the depletion of IFN-$ gamma$ on LPS induced pregnancy loss. The results showed that IFN-$ gamma$ deficient mice were more resistant to LPS induced abortion than control mice. This suggested that IFN-$ gamma$ was essential for the priming of decidual macrophages and that decidual macrophages from IFN-$ gamma$ deficient mice could not be activated when exposed to LPS both in vivo and in vitro. Our results also showed increased IFN-$ gamma$ mRNA expression simultaneously in the same embryos that also expressed elevated iNOS mRNA, a macrophage activation marker. This suggested that macrophage activation, subsequent nitric oxide production, and spontaneous embryo loss could be a consequence of local IFN-$ gamma$ over production.
While LPS serves as an exogenous triggering factor, endogenous TNF-$ alpha$ is known to trigger NO production by primed macrophages. Therefore, we investigated the role of TNF-$ alpha$, as a second signal, in mediating embryo loss. Our studies showed that the frequency of embryos with significantly increased TNF-$ alpha$ mRNA expression corresponded to the incidence of murine embryo abortion. In addition, the results showed that increased TNF-$ alpha$ mRNA was simultaneously expressed with iNOS mRNA suggesting a potential role for TNF-$ alpha$ in the triggering of decidual macrophages.
In summary, we demonstrated the presence of activated decidual macrophages in murine placentas, and that inducible nitric oxide produced by these macrophages was responsible for embryo death. We further showed that IFN-$ gamma$ was responsible for the priming of decidual macrophages, and that the expression of TNF-$ alpha$, a potential secondary signal was associated with decidual macrophage activation, NO production, and subsequent embryo loss.
Warby, Tammra. "Interactions between granulocyte-macrophage colony-stimulating factor and human monocyte-derived macrophages following infection with HIV-1 /". [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19318.pdf.
Pełny tekst źródłaFinney-Hayward, Tricia Kate. "Monocyte-derived macrophages as a lung macrophage model in chronic obstructive pulmonary disease : characterisation and functional output". Thesis, Imperial College London, 2005. http://hdl.handle.net/10044/1/8330.
Pełny tekst źródłaWalter, Michaela Roylene Valerie. "Macrophages in bovine footrot, the effect of Porphyromonas levii on macrophage function and pro-inflammatory cytokine production". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ65143.pdf.
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