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Academic literature on the topic 'Facteur stimulant les colonies de macrophages'
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Journal articles on the topic "Facteur stimulant les colonies de macrophages"
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Whetton, A. D., C. M. Heyworth, S. E. Nicholls, C. A. Evans, J. M. Lord, T. M. Dexter, and P. J. Owen-Lynch. "Cytokine-mediated protein kinase C activation is a signal for lineage determination in bipotential granulocyte macrophage colony-forming cells." Journal of Cell Biology 125, no. 3 (May 1, 1994): 651–59. http://dx.doi.org/10.1083/jcb.125.3.651.
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Granulocyte macrophage colony-forming cells (GM-CFC) have the potential to develop into either macrophages and/or neutrophils. With a highly enriched population of these cells we have found that although GM-CFC are equally responsive to macrophage colony stimulating factor (M-CSF) and stem cell factor (SCF) in terms of DNA synthesis, M-CSF stimulated the development of colonies containing macrophages in soft gel assays, while SCF promoted neutrophilic colony formation. When SCF and M-CSF were combined, mainly macrophage development was stimulated both in soft agar colony-forming assays and liquid cultures. An analysis of some potential signaling mechanisms associated with cytokine-mediated developmental decisions in GM-CFC revealed that M-CSF, but not SCF, was able to chronically stimulate phosphatidylcholine breakdown and diacylglycerol production, indicating that protein kinase C (PKC) may be involved in the action of M-CSF. Furthermore, M-CSF, but not SCF, can increase the levels of PKC alpha (PKC alpha) expression and stimulate the translocation of PKC alpha to the nucleus. When the PKC inhibitor, calphostin C, was added to GM-CFC cultured in M-CSF then predominantly neutrophils were produced, conversely PKC activators added with SCF stimulated macrophage development. The data indicate a role for PKC in M-CSF-stimulated macrophage development from GM-CFC.
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McNiece, IK, BE Robinson, and PJ Quesenberry. "Stimulation of murine colony-forming cells with high proliferative potential by the combination of GM-CSF and CSF-1." Blood 72, no. 1 (July 1, 1988): 191–95. http://dx.doi.org/10.1182/blood.v72.1.191.191.
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Abstract Granulocyte-macrophage colony-stimulating factor (GM-CSF) has previously been shown to stimulate granulocyte, macrophage, and megakaryocyte lineages to act as an erythroid burst-promoting activity and to stimulate limited replication of spleen colony-forming cells. Here we demonstrate that murine GM-CSF alone or in combination with macrophage colony-stimulating factor (CSF-1) can stimulate colony- forming cells in bone marrow (BM) that have a high proliferative capacity. In cultures of BM from mice treated with 5-fluorouracil (FU) eight days before sampling, GM-CSF alone or in combination with CSF-1 stimulated the formation of large macrophage colonies with diameters greater than 0.5 mm. CSF-1 alone, at 800 units or greater, also stimulated larger colonies; however, these colonies were always less than 1.1 mm in diameter, whereas GM-CSF in combination with CSF-1 stimulated many colonies with diameters between 1 and 4 mm. At all doses of CSF-1 tested, the combination of factors resulted in a synergistic increase in colonies with diameters greater than 1.0 or 2.0 mm. Analysis of the incidence of colony-forming cells in the BM of normal mice and mice 2, 4, 6, and 8 days after FU treatment demonstrated that the progenitor cells stimulated by GM-CSF alone or in combination with CSF-1 were depleted by FU treatment in vivo and regenerated more rapidly than did the macrophage progenitors (M-CFC) stimulated by CSF-1 alone. This is similar to the properties of the previously described high-proliferative potential, colony-forming cell (HPP-CFC) that is responsive to interleukin-3 plus CSF-1 but not the HPP-CFC stimulated by hematopoietin 1 plus CSF-1. These data suggest that GM-CSF plus CSF-1 act synergistically to stimulate a population of progenitor cells that have a high proliferative potential and have properties similar to those of the population of HPP-CFC stimulated by interleukin-3 plus CSF-1.
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McNiece, IK, BE Robinson, and PJ Quesenberry. "Stimulation of murine colony-forming cells with high proliferative potential by the combination of GM-CSF and CSF-1." Blood 72, no. 1 (July 1, 1988): 191–95. http://dx.doi.org/10.1182/blood.v72.1.191.bloodjournal721191.
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Granulocyte-macrophage colony-stimulating factor (GM-CSF) has previously been shown to stimulate granulocyte, macrophage, and megakaryocyte lineages to act as an erythroid burst-promoting activity and to stimulate limited replication of spleen colony-forming cells. Here we demonstrate that murine GM-CSF alone or in combination with macrophage colony-stimulating factor (CSF-1) can stimulate colony- forming cells in bone marrow (BM) that have a high proliferative capacity. In cultures of BM from mice treated with 5-fluorouracil (FU) eight days before sampling, GM-CSF alone or in combination with CSF-1 stimulated the formation of large macrophage colonies with diameters greater than 0.5 mm. CSF-1 alone, at 800 units or greater, also stimulated larger colonies; however, these colonies were always less than 1.1 mm in diameter, whereas GM-CSF in combination with CSF-1 stimulated many colonies with diameters between 1 and 4 mm. At all doses of CSF-1 tested, the combination of factors resulted in a synergistic increase in colonies with diameters greater than 1.0 or 2.0 mm. Analysis of the incidence of colony-forming cells in the BM of normal mice and mice 2, 4, 6, and 8 days after FU treatment demonstrated that the progenitor cells stimulated by GM-CSF alone or in combination with CSF-1 were depleted by FU treatment in vivo and regenerated more rapidly than did the macrophage progenitors (M-CFC) stimulated by CSF-1 alone. This is similar to the properties of the previously described high-proliferative potential, colony-forming cell (HPP-CFC) that is responsive to interleukin-3 plus CSF-1 but not the HPP-CFC stimulated by hematopoietin 1 plus CSF-1. These data suggest that GM-CSF plus CSF-1 act synergistically to stimulate a population of progenitor cells that have a high proliferative potential and have properties similar to those of the population of HPP-CFC stimulated by interleukin-3 plus CSF-1.
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Heyworth, CM, TM Dexter, SE Nicholls, and AD Whetton. "Protein kinase C activators can interact synergistically with granulocyte colony-stimulating factor or interleukin-6 to stimulate colony formation from enriched granulocyte-macrophage colony-forming cells." Blood 81, no. 4 (February 15, 1993): 894–900. http://dx.doi.org/10.1182/blood.v81.4.894.894.
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Abstract The effects of direct activators of protein kinase C (PKC) (the phorbol ester tetradecanoyl phorbol myristic acid [TPA] or bryostatin) on the ability of a highly enriched population of granulocyte-macrophage colony-forming cells (GM-CFC) to proliferate and develop in soft agar was assessed. In the absence of colony stimulating factors, the PKC activators did not stimulate colony formation. However, in the presence of optimal concentrations of granulocyte colony-stimulating factor (G- CSF) or interleukin-6 (IL-6), TPA or bryostatin markedly elevated the number of colonies formed from the GM-CFC. In the absence of TPA, IL-6, and G-CSF, respectively, both stimulated the formation of about 3% of the colonies observed when IL-3 was present. When TPA plus G-CSF or IL- 6 were added together, this figure increased to 48% and 54%, respectively. In both instances, the types of mature cells formed was altered from colonies of mature neutrophilic cells to a mixture consisting predominantly of macrophages with some neutrophils. Similar results were observed when bryostatin replaced TPA in these assays. When single cell colony-forming assays were performed, the same results were obtained. The presence of G-CSF, or IL-6, and the activator of PKC used (TPA or bryostatin) was required throughout the colony-forming assay for an optimal synergistic effect to be observed. These data indicate that agents that activate PKC can promote the proliferation and development of GM-CFC via a synergistic interaction with G-CSF or IL-6. Furthermore, there is an apparent role for PKC in development and possibly lineage commitment of GM-CFC.
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Heyworth, CM, TM Dexter, SE Nicholls, and AD Whetton. "Protein kinase C activators can interact synergistically with granulocyte colony-stimulating factor or interleukin-6 to stimulate colony formation from enriched granulocyte-macrophage colony-forming cells." Blood 81, no. 4 (February 15, 1993): 894–900. http://dx.doi.org/10.1182/blood.v81.4.894.bloodjournal814894.
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The effects of direct activators of protein kinase C (PKC) (the phorbol ester tetradecanoyl phorbol myristic acid [TPA] or bryostatin) on the ability of a highly enriched population of granulocyte-macrophage colony-forming cells (GM-CFC) to proliferate and develop in soft agar was assessed. In the absence of colony stimulating factors, the PKC activators did not stimulate colony formation. However, in the presence of optimal concentrations of granulocyte colony-stimulating factor (G- CSF) or interleukin-6 (IL-6), TPA or bryostatin markedly elevated the number of colonies formed from the GM-CFC. In the absence of TPA, IL-6, and G-CSF, respectively, both stimulated the formation of about 3% of the colonies observed when IL-3 was present. When TPA plus G-CSF or IL- 6 were added together, this figure increased to 48% and 54%, respectively. In both instances, the types of mature cells formed was altered from colonies of mature neutrophilic cells to a mixture consisting predominantly of macrophages with some neutrophils. Similar results were observed when bryostatin replaced TPA in these assays. When single cell colony-forming assays were performed, the same results were obtained. The presence of G-CSF, or IL-6, and the activator of PKC used (TPA or bryostatin) was required throughout the colony-forming assay for an optimal synergistic effect to be observed. These data indicate that agents that activate PKC can promote the proliferation and development of GM-CFC via a synergistic interaction with G-CSF or IL-6. Furthermore, there is an apparent role for PKC in development and possibly lineage commitment of GM-CFC.
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Burgess, AW, CG Begley, GR Johnson, AF Lopez, DJ Williamson, JJ Mermod, RJ Simpson, A. Schmitz, and JF DeLamarter. "Purification and properties of bacterially synthesized human granulocyte-macrophage colony stimulating factor." Blood 69, no. 1 (January 1, 1987): 43–51. http://dx.doi.org/10.1182/blood.v69.1.43.43.
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Abstract Human granulocyte-macrophage colony stimulating factor (GM-CSF) has been synthesized in high yield using a temperature inducible plasmid in Escherichia coli. The human GM-CSF is readily isolated from the bacterial proteins because of its differential solubility and chromatographic properties. The bacterially synthesized form of the human GM-CSF contains an extra methionine residue at position 1, but otherwise it is identical to the polypeptide predicted from the cDNA sequence. The specific activity of 2.9 X 10(7) units/mg of protein for purified bacterially synthesized human GM-CSF indicates that despite the lack of glycosylation, the molecule is substantially in its native conformation. This molecule stimulated the same number and type of both seven- and 14-day human bone marrow colonies as the CSF alpha preparation from human placental conditioned medium. Human GM-CSF had no activity on murine bone marrow or murine leukemic cells. There was no detectable, direct stimulation of adult human erythroid burst forming units (BFU-E) by the bacterially synthesized human GM-CSF. Although impure preparations containing native human GM-CSF (eg, human placental conditioned medium) stimulated the formation of mixed colonies, even in the presence of erythropoietin, the bacterially synthesized human GM-CSF failed to stimulate the formation of mixed colonies from adult human bone marrow cells. The bacterially synthesized human GM-CSF increased N-formyl-methionyl-leucyl- phenylalanine (FMLP)-induced superoxide production and lysozyme secretion. Antibody-dependent cytotoxicity and phagocytosis by human neutrophils was stimulated by the bacterially synthesized human GM-CSF and eosinophils were also activated in the antibody-dependent cytotoxicity assay.
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Burgess, AW, CG Begley, GR Johnson, AF Lopez, DJ Williamson, JJ Mermod, RJ Simpson, A. Schmitz, and JF DeLamarter. "Purification and properties of bacterially synthesized human granulocyte-macrophage colony stimulating factor." Blood 69, no. 1 (January 1, 1987): 43–51. http://dx.doi.org/10.1182/blood.v69.1.43.bloodjournal69143.
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Human granulocyte-macrophage colony stimulating factor (GM-CSF) has been synthesized in high yield using a temperature inducible plasmid in Escherichia coli. The human GM-CSF is readily isolated from the bacterial proteins because of its differential solubility and chromatographic properties. The bacterially synthesized form of the human GM-CSF contains an extra methionine residue at position 1, but otherwise it is identical to the polypeptide predicted from the cDNA sequence. The specific activity of 2.9 X 10(7) units/mg of protein for purified bacterially synthesized human GM-CSF indicates that despite the lack of glycosylation, the molecule is substantially in its native conformation. This molecule stimulated the same number and type of both seven- and 14-day human bone marrow colonies as the CSF alpha preparation from human placental conditioned medium. Human GM-CSF had no activity on murine bone marrow or murine leukemic cells. There was no detectable, direct stimulation of adult human erythroid burst forming units (BFU-E) by the bacterially synthesized human GM-CSF. Although impure preparations containing native human GM-CSF (eg, human placental conditioned medium) stimulated the formation of mixed colonies, even in the presence of erythropoietin, the bacterially synthesized human GM-CSF failed to stimulate the formation of mixed colonies from adult human bone marrow cells. The bacterially synthesized human GM-CSF increased N-formyl-methionyl-leucyl- phenylalanine (FMLP)-induced superoxide production and lysozyme secretion. Antibody-dependent cytotoxicity and phagocytosis by human neutrophils was stimulated by the bacterially synthesized human GM-CSF and eosinophils were also activated in the antibody-dependent cytotoxicity assay.
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McNiece, I., R. Andrews, M. Stewart, S. Clark, T. Boone, and P. Quesenberry. "Action of interleukin-3, G-CSF, and GM-CSF on highly enriched human hematopoietic progenitor cells: synergistic interaction of GM-CSF plus G-CSF." Blood 74, no. 1 (July 1, 1989): 110–14. http://dx.doi.org/10.1182/blood.v74.1.110.110.
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Abstract Purified preparations of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte CSF (G-CSF), and interleukin 3 (IL-3 or multi-CSF) alone and in combination, have been compared for their stimulatory effects on human granulocyte-macrophage colony forming cells (GM-CFC). In cultures of unseparated normal human bone marrow, the combinations of G-CSF plus IL-3 and GM-CSF plus IL-3 stimulated additive numbers of GM colonies, while GM-CSF plus G-CSF stimulated greater than additive numbers of GM colonies, compared with the sum of the colony formation obtained with each factor alone. Cultures of unseparated bone marrow, harvested from patients four to six days after administration of 5-fluorouracil (5-FU), resulted in additive GM colony formation with GM-CSF plus G-CSF, GM-CSF plus IL-3, and G-CSF plus IL-3. In order to address the possibility of secondary factor involvement in the synergistic interaction of GM-CSF and G-CSF, CD33+/CD34+ colony forming cells were separated from normal and post FU marrow by two color fluorescence activated cell sorting. In cultures of CD33+/CD34+ cells the combination of GM-CSF plus G-CSF stimulated a synergistic increase in GM colonies while GM-CSF plus IL-3 stimulated additive numbers of colonies. These results suggest that GM-CSF, G-CSF, and IL-3 stimulate distinct populations of GM-CFC. Furthermore GM-CSF and G-CSF interact synergistically and this action is a direct effect on progenitor cells not stimulated by GM-CSF or G-CSF alone.
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McNiece, I., R. Andrews, M. Stewart, S. Clark, T. Boone, and P. Quesenberry. "Action of interleukin-3, G-CSF, and GM-CSF on highly enriched human hematopoietic progenitor cells: synergistic interaction of GM-CSF plus G-CSF." Blood 74, no. 1 (July 1, 1989): 110–14. http://dx.doi.org/10.1182/blood.v74.1.110.bloodjournal741110.
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Purified preparations of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte CSF (G-CSF), and interleukin 3 (IL-3 or multi-CSF) alone and in combination, have been compared for their stimulatory effects on human granulocyte-macrophage colony forming cells (GM-CFC). In cultures of unseparated normal human bone marrow, the combinations of G-CSF plus IL-3 and GM-CSF plus IL-3 stimulated additive numbers of GM colonies, while GM-CSF plus G-CSF stimulated greater than additive numbers of GM colonies, compared with the sum of the colony formation obtained with each factor alone. Cultures of unseparated bone marrow, harvested from patients four to six days after administration of 5-fluorouracil (5-FU), resulted in additive GM colony formation with GM-CSF plus G-CSF, GM-CSF plus IL-3, and G-CSF plus IL-3. In order to address the possibility of secondary factor involvement in the synergistic interaction of GM-CSF and G-CSF, CD33+/CD34+ colony forming cells were separated from normal and post FU marrow by two color fluorescence activated cell sorting. In cultures of CD33+/CD34+ cells the combination of GM-CSF plus G-CSF stimulated a synergistic increase in GM colonies while GM-CSF plus IL-3 stimulated additive numbers of colonies. These results suggest that GM-CSF, G-CSF, and IL-3 stimulate distinct populations of GM-CFC. Furthermore GM-CSF and G-CSF interact synergistically and this action is a direct effect on progenitor cells not stimulated by GM-CSF or G-CSF alone.
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Hestdal, K., SE Jacobsen, FW Ruscetti, CM Dubois, DL Longo, R. Chizzonite, JJ Oppenheim, and JR Keller. "In vivo effect of interleukin-1 alpha on hematopoiesis: role of colony- stimulating factor receptor modulation." Blood 80, no. 10 (November 15, 1992): 2486–94. http://dx.doi.org/10.1182/blood.v80.10.2486.2486.
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Abstract To determine the mechanism(s) by which interleukin-1 (IL-1) promotes granulopoiesis in vivo, we examined the effect of in vivo administration of IL-1 alpha on colony-stimulating factor (CSF) receptor expression on bone marrow cells (BMCs) and whether this directly correlated with progenitor cell responsiveness. Administration of IL-1 alpha to mice induced the upregulation of both granulocyte- macrophage-CSF (GM-CSF) and IL-3 receptors, which reached a maximum 24 hours after IL-1 alpha injection on unfractionated BMCs. This upregulation was more pronounced on the progenitor-enriched cell population (lineage-negative [Lin(-)]). The enhanced GM-CSF and IL-3 receptor expression directly correlated with enhanced IL-3- or GM-CSF- induced growth of colony-forming unit-culture (CFU-c) or CFU-mixture (CFU-Mix; colonies containing macrophages, granulocytes, and erythroid cells). In addition, the absolute number of high proliferative potential-colony-forming cells (HPP-CFC) was increased fivefold. In contrast, granulocyte-CSF (G-CSF)-specific binding on unfractionated BMCs was rapidly (4 hours) reduced after IL-1 alpha administration and returned to control levels by 24 hours. This reduction correlated with IL-1 alpha-induced margination of mature granulocytes (RBC-8C5hi cells), which express high levels of G-CSF receptors. IL-1 alpha treatment did not affect G-CSF receptor expression on Lin- cells. Pretreatment of mice with anti-type I IL-1 receptor antibody blocked the IL-1 alpha-induced upregulation of GM-CSF and IL-3 receptor expression on BMCs. Taken together, as one possible mechanism, IL-1 alpha in vivo may stimulate the expression of functional GM-CSF and IL- 3 receptors on BMCs indirectly, and, in concert with the induction of circulating CSF levels, may account for the ability of IL-1 alpha to stimulate hematopoiesis in vivo.
Dissertations / Theses on the topic "Facteur stimulant les colonies de macrophages"
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Pons, Vincent. "Rôle du CSF1R dans les maladies neurodégénératives." Doctoral thesis, Université Laval, 2021. http://hdl.handle.net/20.500.11794/68078.
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Breton, Yann. "Rôle du facteur de transcription p53 dans l'infection des macrophages humains par le VIH-1." Doctoral thesis, Université Laval, 2021. http://hdl.handle.net/20.500.11794/68547.
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Gowing, Geneviève. "Le rôle de l'inflammation et des microglies dans la sclérose latérale amyotrophique." Thesis, Université Laval, 2009. http://www.theses.ulaval.ca/2009/26199/26199.pdf.
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Karlin, Lionel Azoulay Elie. "Détérioration respiratoire en sortie d'aplasie sous facteur de croissance hématopoïétique (G-CSF) à propos de 20 cas /." Créteil : Université Paris-Val-de-Marne, 2004. http://doxa.scd.univ-paris12.fr:80/theses//th0222006.pdf.
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El, Hajj Dib-Zakaria Iman. "Régulation de l'apoptose des ostéoclastes matures par les plasmocytes tumoraux : implication dans l'ostéolyse du myélome multiple." Amiens, 2007. http://www.theses.fr/2007AMIED014.
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Le myélome multiple (MM) est une hémopathie maligne définie par une infiltration plasmocytaire médullaire. 80% des patients atteints, présentent au moment du diagnostic, des lésions osseuses aggravant la maladie. L’augmentation du nombre d’ostéoclastes actifs est le principal déterminant dans la pathogenèse de ces lésions. Il est clairement établi aujourd’hui que les cellules de MM stimulent la différenciation ostéoclastique à l’origine d’une augmentation de la résorption osseuse. Cependant, à ce jour, aucune donnée n’est disponible concernant l’aptitude de ces cellules à réguler l’apoptose des ostéoclastes, un mécanisme qui contribue fortement à réguler le nombre d’ostéoclastes actifs. C’est pourquoi, dans ce travail nous avons testé les effets des milieux conditionnés (MC) préparés à partir de plasmocytes tumoraux à la fois sur l’activité de résorption ostéoclastique et sur l’apoptose des ostéoclastes. A l’aide d’un modèle d’ostéoclastes matures de lapin, nous démontrons que les MC stimulent la résorption osseuse ostéoclastique et inhibent simultanément l’apoptose des ostéoclastes. Le dosage des principaux facteurs de survie ostéoclastique dans les MC, montre que seul le macrophage colony stimulating factor (M-CSF) est secrété dans des quantités compatibles avec un effet antiapoptotique. L’implication du M-CSF a été confirmée à l’aide d’un anticorps neutralisant dirigé contre le M-CSF. Pour supporter ces données expérimentales, une étude clinique préliminaire nous a permis de démontrer que la moyenne des concentrations sériques de M-CSF chez les patients atteints de MM (n =33) est significativement plus élevée comparativement aux sujets témoins (n= 34) et que les taux de M-CSF sont significativement corrélés avec le degré de l’atteinte osseuse. Enfin, nous montrons que le mésylate d’imatinib (gleevec®), un inhibiteur des récepteurs à activités tyrosine kinase, est capable de bloquer à la fois les effets anti-apoptotiques et les effets stimulateurs de la résorption, exercés par les MC sur les ostéoclastes matures. L’ensemble de nos résultats suggère que le M-CSF sécrété par les cellules de MM joue un rôle central dans l’ostéolyse du myélome multiple et constitue une cible thérapeutique de choix dans le traitement de l’atteinte osseuse du myélomeMultiple myeloma (MM) is characterized by devastating bone destruction mainly due to stimulation of osteoclastogenesis. However, whether MM cells can influence osteoclast apoptosis, a mechanism that contributes to the increase in the number of active osteoclasts, has not been adressed yet. In this study, we assessed the effects of MM cells on osteoclast bone resorbing activity and apoptosis and we attempted to identify the anti-apoptotic factors originating from MM cells. Conditioned media (CM) were collected from different human MM cells and we assessed their ability to stimulate bone resorbing activity and to influence apoptosis using a cell model of authentic mature rabbit osteoclast. We found that CM potently stimulated bone resorption and inhibited osteoclast apoptosis in a dose-dependent manner. We demonstrated that MM cells, which exerted an anti-apoptotic effect, secreted high amounts of M-CSF and addition of a neutralizing antibody against M-CSF reversed the CM effects. Imatinib mesylate (gleevec®), a tyrosine kinase inhibitor that targets the M-CSF receptor, also prevented the effect of CM on both osteoclast apoptosis and bone resorbing activity. Consistently, serum levels of M-CSF in MM patients (n = 33) were significantly increased as compared to control subjects (n = 34) and positively correlated with the presence of bone lesions. Based on these findings, we conclude that M-CSF originating from MM cells may play a critical role in MM bone disease by decreasing osteoclast apoptosis at local sites. Blockade of M-CSF signalling pathway may constitute a new therapeutic approach in the treatment of myeloma bone disease
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Ségaliny, Aude. "Biologie de l'interleukine-34 et rôle dans la pathogenèse de l'ostéosarcome." Nantes, 2014. http://archive.bu.univ-nantes.fr/pollux/show.action?id=da1cd31e-d4a6-4013-91bb-7ad9ba56cf15.
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Surexprimé dans de nombreux cancers, le M-CSF se révèle être facteur de mauvais pronostic, et favorise l'initiation, la croissance et la dissémination tumorale. En 2008, une nouvelle cytokine, l'IL-34, a été identifiée comme facteur de survie monocytaire et de différenciation macrophagique/ostéoclastique, pouvant ainsi se substituer au M-CSF. Son implication a également été décrite dans certaines pathologies osseuses comme les tumeurs à cellules géantes, la polyarthrite rhumatoïde ou les maladies parodontales. Néanmoins, le rôle de l'IL-34 dans l'ostéosarcome n'a à ce jour jamais été décrit. Par ailleurs, ces cytokines « jumelles » homodimériques sont en compétition sur un récepteur commun, le M-CSFR, bien qu'un autre récepteur à l'IL-34 ait récemment été identifié. Ces travaux se sont donc intéressés aux interrelations fonctionnelles entre le M-CSF, l'IL-34 et le M-CSFR. Tout d'abord, nous avons pu montrer que l'IL-34 était exprimée dans les tumeurs de patients atteints d'ostéosarcome, et que la cytokine favorisait la progression tumorale et le développement métastatique in vivo dans un modèle murin d'ostéosarcome, via l'angiogenèse et le recrutement de macrophages tumoraux. Ensuite, nous avons mis en évidence avec des études plus fondamentales l'existence d'une autre chaîne réceptrice pour l'IL-34, le syndécan-1, capable de moduler l'activation du M-CSFR induite par l'IL-34. Pour finir, l'IL-34 est capable de former une cytokine hétéromérique fonctionnelle avec sa jumelle, le M-CSF. En conclusion, la biologie de l'IL-34 est très complexe et met en jeu différents acteurs moléculaires qu'il faudra prendre en compte pour le développement de futures thérapiesM-CSF is highly expressed in several cancers and is often associated with a bad prognosis, as its expression correlates with increased tumor initiation, growth and metastasis. Discovered in 2008, IL-34 is a challenging cytokine that regulates, like M-CSF, the survival, proliferation and differentiation of mononuclear phagocytes. Furthermore, IL-34 is involved in some bone diseases such as giant-cell tumour of bone, rheumatoid arthritis or periodontitis. However, IL-34 role in osteosarcoma has never been described. Besides, the “twin” cytokines are homodimers known to bind to the M-CSFR in a competitive manner, even another receptor was identified more recently for IL-34. The aim of the present work was also to study the functional relationships of these cytokines and to look for an alternative binding for IL-34. First, we demonstrated that IL-34 was expressed in tumours of patients who suffered from osteosarcoma. In addition, IL-34 promoted tumour growth and metastasis through angiogenesis development and macrophages recruitment in tumour microenvironment in an in vivo murine model of osteosarcoma. In a second part, this work evidenced novel and original functional mechanisms in the M-CSF/IL-34/M-CSFR triad. Indeed, IL-34 is able to bind to syndecan-1, thereby modulating the M-CSFR activation. In addition, IL-34 and M-CSF are able to form a new heteromeric cytokine, biologically active. To conclude, these functional interactions and new partners should be further analyzed in pathophysiological contexts and should be taken into account in new treatments development
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Bellomo, Alicia. "Contrôle de l’homéostasie des macrophages de la pulpe rouge splénique par une niche fibroblastique." Thesis, Aix-Marseille, 2020. http://www.theses.fr/2020AIXM0197.
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Situés dans les cordons de Billroth de la rate, les macrophages de la pulpe rouge (RPM) sont continuellement exposés au flux du sang. Leur fonction principale est d’éliminer les globules rouges sénescents et de recycler le fer contenu dans leur hémoglobine. Les cellules dites« stromales » sont des cellules de soutien qui constituent des niches pour les macrophages de différents organes. Au cours de mon travail de thèse, j’ai étudié les mécanismes qui régulent l'homéostasie des RPM en me focalisant sur la contribution des cellules stromales. En utilisant différentes techniques d’imagerie, j’ai révélé que les RPM sont enchâssés dans un réseau réticulaire de fibroblastes caractérisés par l'expression de la protéine de la tumeur de Wilm 1(WT1) et le facteur de stimulation des colonies de macrophages 1 (CSF1). La délétion conditionnelle du gène Csf1 dans les fibroblastes de la pulpe rouge exprimant WT1, mais pasdans les fibroblastes de la pulpe blanche, réduit drastiquement le nombre de RPM sans modifier le niveau de CSF1 circulant. Suite à la déplétion des RPM, les fibroblastes de la pulpe rougeproduisent de manière transitoire les facteurs chimiotactiques pour les monocytes CCL2 et CCL7et de fait contribuent à la reconstitution de la population de RPM. Ainsi, les fibroblastes de la pulpe rouge soutiennent et nourrissent les RPM, une fonction qui est vraisemblablement conservée chez l'hommeLocated within red pulp cords, splenic red pulp macrophages (RPM) are constantly exposed tothe blood flow, clearing senescent red blood cells (RBC) and recycling iron from hemoglobin.Here, we studied the mechanisms underlying RPM homeostasis, focusing on the involvement ofstromal cells as these cells perform anchoring and nurturing macrophage niche functions inlymph nodes and liver. Microscopy revealed that RPM are embedded in a reticular meshwork ofred pulp fibroblasts characterized by the expression of Wilm’s Tumor 1 (WT1) and colonystimulating factor 1 (CSF1). Conditional deletion of Csf1 in WT1+ red pulp fibroblasts, but notwhite pulp fibroblasts, drastically altered the RPM network without altering circulating CSF1levels. Upon RPM depletion, red pulp fibroblasts transiently produced the monocytechemoattractants CCL2 and CCL7, thereby contributing to the replenishment of the RPMnetwork. Thus, red pulp fibroblasts anchor and nurture RPM, a function likely conserved inhumans
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Gallet, Marlène. "Influence des cellules d'adénocarcinome mammaire sur la résorption osseuse et l'apoptose des ostéoclastes matures : rôle potentiel du M-CSF dans l'ostéolyse tumorale in vitro." Paris 7, 2006. http://www.theses.fr/2006PA077103.
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La complication majeure du cancer du sein est l'apparition de métastases notamment au niveau du tissu osseux. Ces métastases osseuses sont responsables d'une osteolyse importante due à une activation accrue des ostéoclastes. Nous nous sommes intéressés aux mécanismes impliqués dans la modulation de la résorption osseuse et de l'apoptose des ostéoclastes matures par les cellules d'adénocarcinome mammaire. Nous avons montré que les facteurs sécrétés par les cellules de la lignée MDA-MB-231 inhibent l'apoptose des ostéoclastes et stimulent la résorption osseuse. Après avoir mis en évidence l'implication majeure de la voie des PI3 kinases et du M-CSF dans l'effet anti-apoptotique induit par les cellules cancéreuse du sein, nous avons montré une corrélation entre le potentiel ostéolytique in vitro de différentes lignées de cancer du sein e leur capacité à produire le M-CSF. Deux approches visant à diminuer les effets du M-CSF ont été évaluées. La première approche a consisté à bloquer l'activation du récepteur du M-CSF, le c-fms par l'emploi de l'imatinib. La seconde approche a consisté à diminuer la production du M-CSF au niveau des cellules cancéreuses du sein par l'interférence à l'ARN et par l'utilisation de SERM (modulateurs sélectifs des récepteurs des estrogènes). Des études in vivo permettront de confirmer l'intérêt thérapeutique de ces deux stratégies pour le traitement de l'ostéolyse qui accompagne le développement métastatique osseux du cance du seinThe most common complication of breast carcinoma is bone metastasis which is responsible for osteolysis due mainly to a great activation of osteoclastic bone resorption. Herein, we investigated the mechanism implicated in the modulation of bone resorption and mature osteoclast apoptosis by breast carcinoma cells. We showed that soluble factors released by MDA-MB-231 cells decreased osteoclast apoptosis and increased bone resorption. We specified that Pl3 kinase pathway and M-CSF are involved in the breast cancer cell-induced anti-apoptotic effect. Then we demonstrated a correlation between osteolytic potential of breast carcinoma cell lines and their capacity to produce M-CSF. In order to decrease the effects of M-CSF on osteoclast, we used two strategies. The first consisted to block the M-CSF receptor activation in osteoclast by using imatinib and the second consisted to reduce the M-CSF production in breast cancer cells using RNA interference and SERM (Selective Estrogen Receptor Modulator) treatments. Further in vivo investigations would confirm their therapeutic interest in the treatment of breast carcinoma related bone metastasis
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Vereecque, Rodolphe. "Transfert de gènes ou thérapie celllulaire : applications à l'immunothérapie des leucémies aigües myéloi͏̈des." Lille 1, 2000. https://pepite-depot.univ-lille.fr/RESTREINT/Th_Num/2000/50376-2000-492.pdf.
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Environ 1000 nouvelles leucemies aigues sont diagnostiquees par an en france. Le traitement repose essentiellement sur la polychimiotherapie et dans certains cas, la greffe medullaire. Toutefois il persiste le plus souvent chez une majorite de patients un faible contingent de cellules leucemiques, responsable des rechutes. Le pronostic est lie essentiellement a la probabilite de rechute, fortement correlee a la persistance de la maladie residuelle. Le developpement de nouvelles approches therapeutiques semble constituer la seule alternative permettant de palier les taux de rechutes observes apres chimiotherapie. Contrairement aux tumeurs solides, la possibilite d'obtenir un grand nombre de cellules tumorales des le diagnostic permet leur modification ex vivo en vue d'une utilisation en therapie genique ou cellulaire. Dans ce contexte, nous avons developpe un modele murin syngenique de leucemie aigue afin de valider l'approche therapeutique par transfert de genes. Les souris syngeniques c3h injectees par un faible nombre de cellules da1 3b, exprimant le gene de fusion bcr-abl, developpent rapidement une leucemie aigue (mediane de survie 20 jours pour 10 4 cellules injectees). Le transfert des genes du gm-csf, du cd80 et du cd154, seuls ou en associations, dans la lignee da1 3b, permet d'eradiquer une leucemie preetablie chez l'animal. La persistance d'une maladie residuelle chez les souris survivantes suggere que la vaccination par des cellules leucemiques modifiees puisse induire un phenomene de latence tumorale compatible avec la survie a long terme.
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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 TAMIn 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
Books on the topic "Facteur stimulant les colonies de macrophages"
1
Gregory, Bock, and Goode Jamie, eds. The molecular basis of cellular defence mechanisms. Chichester: Wiley, 1997.
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2
Symposium, CIBA Foundation. The Molecular Basis of Cellular Defence Mechanisms - Symposium No. 204. John Wiley & Sons, 1997.
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