Relevant bibliographies by topics / Monocytes – immunologie

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Monocytes – immunologie'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Monocytes – immunologie"

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Yourno, J., P. Burkart, W. Mastropaolo, F. Lizzi, and A. Tartaglia. "Monocyte nonspecific esterase. Enzymologic characterization of a neutral serine esterase associated with myeloid cells." Journal of Histochemistry & Cytochemistry 34, no. 6 (June 1986): 727–33. http://dx.doi.org/10.1177/34.6.3457861.

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Monocytes contain a characteristic, prominent set of membrane-bound nonspecific esterases with a slightly acid isoelectric point. These esterases are also detected at modest levels in some granulocyte preparations. They are not apparent in lymphocytes. Among 18 fresh myeloid leukemias and myeloid leukemia cell lines, those of subtypes M4 (myelomonocytic) and M5 (monocytic) were strongly positive; some of subtypes M1-M3 (granulocytic) were moderately positive. The esterases were not detected among 32 fresh lymphoid leukemias and lymphoid leukemia and lymphoblast cell lines. The membrane-bound monocyte esterases, solubilized by treatment of monocyte preparations with nonionic detergent, were resolved by ion-exchange chromatography. The monocyte species account for 80-95% of the total nonspecific esterase activity of monocytes. The resolved enzymes behave as neutral serine carboxyl esterases and are highly sensitive to inhibition by diisopropylfluorophosphate (DFP) and also by sodium fluoride. Similar analysis of a lymphocyte preparation yielded no detectable monocyte esterases, but yielded numerous other forms which were generally resistant to inhibition by DFP and NaF. These nonspecific esterases are also present at background levels in monocytes. The resolution and characterization of the membrane-bound serine esterases from monocytes demonstrates the basis for the well-known cytochemistry of monocytes. The results are also crucial to the development of an immunologic surface marker test for myeloid cells and the study of monocyte membrane physiology.
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Zachariae, C. O., A. O. Anderson, H. L. Thompson, E. Appella, A. Mantovani, J. J. Oppenheim, and K. Matsushima. "Properties of monocyte chemotactic and activating factor (MCAF) purified from a human fibrosarcoma cell line." Journal of Experimental Medicine 171, no. 6 (June 1, 1990): 2177–82. http://dx.doi.org/10.1084/jem.171.6.2177.

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A monocyte chemotactic and activating factor (MCAF) has been purified from TNF-stimulated 8387 human fibrosarcoma cell line-conditioned media. The purified MCAF showed microheterogeneity yielding two bands on SDS-PAGE analysis. Fibrosarcoma-derived MCAF specifically competed with THP-1 (a human monocytic cell line)-derived 125I-labeled MCAF in binding to human PBMC, whereas a similar basic heparin-binding leukocyte chemoattractant, IL-8, did not. The purified MCAF stimulated superoxide anion and N-acetyl beta-D glucosaminidase-releasing activity in human monocytes, as well as monocyte cytostatic augmenting activity against tumor cells and chemotactic activity for monocytes. When injected subcutaneously into Lewis rat ears, the purified human MCAF also induced considerable in vivo local monocyte infiltration beginning at 3 h and becoming maximal at 18 h. In conclusion, the data presented in this paper indicate that MCAF is a potent activator of monocytes as well as a monocyte recruitment factor that acts through receptors that are specific for this novel molecule. This novel cytokine might have an important role in tumor growth control due to its ability to attract and activate monocytes.
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Schroff, RW, MM Farrell, RA Klein, HC Stevenson, and NL Warner. "Induction and enhancement by monocytes of antibody-induced modulation of a variety of human lymphoid cell surface antigens." Blood 66, no. 3 (September 1, 1985): 620–26. http://dx.doi.org/10.1182/blood.v66.3.620.620.

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Abstract We have previously reported that the addition of monocytes results in enhanced modulation of the T65 antigen when normal or leukemic lymphoid cells were cultured in vitro with the T101 monoclonal antibody. In the present investigation, we extend these findings to demonstrate that monocyte-enhanced modulation is a phenomenon that occurs with a variety of T and B lymphoid antigens identified by murine monoclonal antibodies. Two patterns of monocyte-enhanced modulation were observed: (1) augmentation by monocytes of existing antigen modulation by the T101 and anti-Leu-4 antibodies, and (2) induction by monocytes of previously unrecognized modulation with the anti-Leu-2 and anti-Leu-9 antibodies. Enhancement of modulation by monocytes was also detected with antibodies to surface IgM and HLA-DR antigens. Antigen modulation on lymphoid cell lines appeared to be more variable than on fresh cells, with or without monocytes. Monocyte-enhanced antigen modulation was not demonstrated with two monoclonal antibodies against solid tumors. Monocyte-enhanced modulation was shown to be dependent upon the Fc portion of the antibody, but independent of proteolytic or oxidative compounds released by monocytes. These findings indicate that the results obtained during in vitro studies of antigen modulation may vary with the source of cells and the extent to which monocytic cells are present. In addition, these findings suggest an enhanced role for Fc receptor-bearing cells of monocytic origin in antigen modulation following in vivo administration of monoclonal antibodies.
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Schroff, RW, MM Farrell, RA Klein, HC Stevenson, and NL Warner. "Induction and enhancement by monocytes of antibody-induced modulation of a variety of human lymphoid cell surface antigens." Blood 66, no. 3 (September 1, 1985): 620–26. http://dx.doi.org/10.1182/blood.v66.3.620.bloodjournal663620.

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We have previously reported that the addition of monocytes results in enhanced modulation of the T65 antigen when normal or leukemic lymphoid cells were cultured in vitro with the T101 monoclonal antibody. In the present investigation, we extend these findings to demonstrate that monocyte-enhanced modulation is a phenomenon that occurs with a variety of T and B lymphoid antigens identified by murine monoclonal antibodies. Two patterns of monocyte-enhanced modulation were observed: (1) augmentation by monocytes of existing antigen modulation by the T101 and anti-Leu-4 antibodies, and (2) induction by monocytes of previously unrecognized modulation with the anti-Leu-2 and anti-Leu-9 antibodies. Enhancement of modulation by monocytes was also detected with antibodies to surface IgM and HLA-DR antigens. Antigen modulation on lymphoid cell lines appeared to be more variable than on fresh cells, with or without monocytes. Monocyte-enhanced antigen modulation was not demonstrated with two monoclonal antibodies against solid tumors. Monocyte-enhanced modulation was shown to be dependent upon the Fc portion of the antibody, but independent of proteolytic or oxidative compounds released by monocytes. These findings indicate that the results obtained during in vitro studies of antigen modulation may vary with the source of cells and the extent to which monocytic cells are present. In addition, these findings suggest an enhanced role for Fc receptor-bearing cells of monocytic origin in antigen modulation following in vivo administration of monoclonal antibodies.
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von Hundelshausen, Philipp, Rory R. Koenen, Markus Sack, Sebastian F. Mause, Wencke Adriaens, Amanda E. I. Proudfoot, Tilman M. Hackeng, and Christian Weber. "Heterophilic interactions of platelet factor 4 and RANTES promote monocyte arrest on endothelium." Blood 105, no. 3 (February 1, 2005): 924–30. http://dx.doi.org/10.1182/blood-2004-06-2475.

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AbstractThe chemokines platelet factor 4 (PF4) and RANTES (regulated on activation normal T cell expressed and secreted) are secreted by activated platelets and influence multiple cell types and biologic processes. For instance, PF4 inhibits progenitor cell proliferation and angiogenesis, while platelet-derived RANTES is involved in vascular recruitment of monocytes. However, little is known about functional interactions of PF4 and RANTES. Here we show that the presence of PF4 enhanced the arrest of RANTES-stimulated monocytes and monocytic cells on activated endothelial cells under flow conditions, while binding of PF4 to the monocyte surface was increased by RANTES. Both RANTES-triggered arrest and PF4 binding involved monocytic chondroitin sulfate. Ligand blots and surface plasmon resonance revealed a robust heterophilic interaction of PF4 with RANTES but not with RANTES variants defective in higher order oligomerization. The tetrameric mutant E26A bound to the monocyte surface without increasing PF4 binding, and monocyte arrest induced by E26A-RANTES was not enhanced by PF4. Stimulation of monocytes with supernatants of activated platelets triggered arrest involving RANTES and PF4, as shown by inhibition studies. Our results suggest that heterophilic interactions with PF4 require structural motifs important in RANTES oligomerization and amplify RANTES-triggered effects on monocyte adhesion. This may have implications for the modulation of inflammatory recruitment by platelet-derived chemokines.
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Zawada, Adam M., Kyrill S. Rogacev, Björn Rotter, Peter Winter, Rolf-R. Marell, Danilo Fliser, and Gunnar H. Heine. "SuperSAGE evidence for CD14++CD16+ monocytes as a third monocyte subset." Blood 118, no. 12 (September 22, 2011): e50-e61. http://dx.doi.org/10.1182/blood-2011-01-326827.

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Abstract Monocytes are a heterogeneous cell population with subset-specific functions and phenotypes. The differential expression of CD14 and CD16 distinguishes classical CD14++CD16−, intermediate CD14++CD16+, and nonclassical CD14+CD16++ monocytes. Current knowledge on human monocyte heterogeneity is still incomplete: while it is increasingly acknowledged that CD14++CD16+ monocytes are of outstanding significance in 2 global health issues, namely HIV-1 infection and atherosclerosis, CD14++CD16+ monocytes remain the most poorly characterized subset so far. We therefore developed a method to purify the 3 monocyte subsets from human blood and analyzed their transcriptomes using SuperSAGE in combination with high-throughput sequencing. Analysis of 5 487 603 tags revealed unique identifiers of CD14++CD16+ monocytes, delineating these cells from the 2 other monocyte subsets. Gene Ontology (GO) enrichment analysis suggests diverse immunologic functions, linking CD14++CD16+ monocytes to Ag processing and presentation (eg, CD74, HLA-DR, IFI30, CTSB), to inflammation and monocyte activation (eg, TGFB1, AIF1, PTPN6), and to angiogenesis (eg, TIE2, CD105). In conclusion, we provide genetic evidence for a distinct role of CD14++CD16+ monocytes in human immunity. After CD14++CD16+ monocytes have earlier been discussed as a potential therapeutic target in inflammatory diseases, we are hopeful that our data will spur further research in the field of monocyte heterogeneity.
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Surdacki, Andrzej, Joanna Sulicka, Mariusz Korkosz, Tomasz Mikołajczyk, Dorota Telesińska-Jasiówka, Ewa Klimek, Izabella Kierzkowska, Tomasz Guzik, and Tomasz K. Grodzicki. "Blood Monocyte Heterogeneity and Markers of Endothelial Activation in Ankylosing Spondylitis." Journal of Rheumatology 41, no. 3 (February 1, 2014): 481–89. http://dx.doi.org/10.3899/jrheum.130803.

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Objective.Ankylosing spondylitis (AS) is associated with excessive cardiovascular (CV) morbidity. Interactions between activated endothelium and monocytes precede atherosclerotic plaques. Our aim was to quantify blood monocyte subsets in relation to endothelial activation and inflammatory activity in subjects with AS who were free of clinical atherosclerotic CV disease.Methods.Markers of inflammation and endothelial activation were measured in 47 patients with AS receiving no disease-modifying antirheumatic drugs, and 22 healthy controls. Exclusion criteria included atherosclerotic CV disease and traditional risk factors. Flow cytometry was used to identify monocyte subsets: classical CD14++CD16−, intermediate CD14++CD16+, and nonclassical CD14+CD16++monocytes and to evaluate their expression of CD11b and CD11c.Results.Traditional risk factors were comparable among the groups, except for lower high-density lipoprotein cholesterol in AS (p = 0.007). Relative to controls, in subjects with AS counts of classical monocytes were higher (84.3 ± 5.4 vs 78.9 ± 5.3% of blood monocytes, p < 0.001) and nonclassical monocytes lower (2.9 ± 2.2 vs 5.5 ± 2.3%, p < 0.001). In AS we observed increased soluble intercellular adhesion molecule-1 [251 (224–293) vs 202 (187–230) ng/ml, p = 0.002], an endothelial ligand for monocytic β2-integrin CD11b/CD18. CD11b expression on all 3 monocyte subsets was elevated in 21 AS subjects with a Bath Ankylosing Spondylitis Disease Activity Index score ≥ 4 versus the remaining patients (p = 0.005–0.03). C-reactive protein, interleukin 6 (IL-6), and pentraxin-3 were increased in AS, in contrast to tumor necrosis factor-α and IL-18. IL-6 correlated with classical monocytes numbers in AS (r = 0.56, p < 0.0001) but not in the controls (r = 0.10, p = 0.65).Conclusion.Our findings suggest a contribution of immune dysregulation to enhanced monocyte-endothelial interactions in AS, especially in patients with active disease, which possibly can accelerate atherogenesis on a longterm basis.
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Jansen, J. H., J. C. Kluin-Nelemans, J. Van Damme, G. J. Wientjens, R. Willemze, and W. E. Fibbe. "Interleukin 6 is a permissive factor for monocytic colony formation by human hematopoietic progenitor cells." Journal of Experimental Medicine 175, no. 4 (April 1, 1992): 1151–54. http://dx.doi.org/10.1084/jem.175.4.1151.

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Since monocytes and macrophages that arise during the culture of bone marrow progenitor cells are potential sources of interleukin 6 (IL-6), we investigated whether auto- or paracrine production of this factor is involved in colony formation by normal hematopoietic progenitor cells. We added a polyclonal anti-IL-6 antiserum and a monoclonal anti-IL-6 antibody to cultures of monocyte- and T cell-depleted bone marrow cells. Colony formation was stimulated with granulocyte/monocyte-colony-stimulating factor (GM-CSF), monocyte-CSF, or IL-3. Addition of anti-IL-6 antibody resulted in decreased numbers of monocytic colonies to 40-50% of control values, whereas the numbers of granulocytic colonies were not altered. The inhibitory effect was preserved in cultures of CD34(+)-enriched bone marrow cells. As a second approach, we added a monoclonal antibody directed against the IL-6 receptor to cultures of monocyte- and T cell-depleted bone marrow cells. This antibody almost completely inhibited the growth of monocytic colonies, again without decreasing the number of granulocytic colonies. Finally, the importance of IL-6 in monocytopoiesis was demonstrated in serum-deprived bone marrow cultures: addition of exogenous IL-6 to cultures stimulated with GM-CSF resulted in increased numbers of monocytic colonies. Our results indicate that the permissive presence of IL-6 is required for optimal monocytic colony formation by bone marrow progenitor cells.
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Oeth, Paul, Jin Yao, Sao-Tah Fan, and Nigel Mackman. "Retinoic Acid Selectively Inhibits Lipopolysaccharide Induction of Tissue Factor Gene Expression in Human Monocytes." Blood 91, no. 8 (April 15, 1998): 2857–65. http://dx.doi.org/10.1182/blood.v91.8.2857.2857_2857_2865.

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Expression of tissue factor (TF) by activated monocytes in several diseases leads to disseminated intravascular coagulation. Lipopolysaccharide (LPS)-induced monocyte TF expression is downregulated by the nuclear hormone all-trans retinoic acid (ATRA). In this study, we examined the mechanism by which ATRA inhibits monocyte TF expression. We show that ATRA selectively inhibited LPS induction of TF expression in human monocytes and monocytic THP-1 cells without affecting LPS induction of tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8). Inhibition of TF expression occurred at the level of transcription as determined by nuclear run-on. ATRA did not significantly alter the binding or functional activity of the transcription factors c-Fos/c-Jun and c-Rel/p65, which are required for LPS induction of the TF promoter in monocytic cells. In contrast to the ATRA inhibition of the endogenous TF gene, LPS induction of the cloned TF promoter was not inhibited by ATRA in transiently transfected THP-1 cells. Our results demonstrate that ATRA selectively inhibited LPS-induced TF gene transcription in human monocytic cells by a mechanism that does not involve repression of AP-1– or NF-κB–mediated transcription.
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Park, In-Woo, Appakkudal R. Anand, and Jerome E. Groopman. "Molecular Characterization of the Cannabinoid-Mediated Migration of Monocytes." Blood 106, no. 11 (November 16, 2005): 3878. http://dx.doi.org/10.1182/blood.v106.11.3878.3878.

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Abstract 2-Arachidonoylglycerol (2-AG), an endogenous ligand for the cannabinoid receptors CB1 and CB2, functions as a chemokine for monocyte migration. However, the molecular mechanism of its chemotactic effects is not clear. We found, consistent with previous data, that 2-AG induces the migration of differentiated but not undifferentiated monocytic cells in a dose-dependent manner. We first asked whether the expression of cannabinoid receptors changed during monocytic differentiation. Treatment with 1,25-(OH)2vitamin D3, a potent inducer of monocyte differentiation, or with 2-AG did not alter the surface expression of the CB1 and CB2 receptors, indicating that signaling downstream of receptor ligation accounted for the observed effect on monocyte migration. In addition, treatment of differentiated monocytic cells with inhibitors for adenyl cyclase and rho kinase blocked the 2-AG-mediated migration, directly implicating these signaling molecules in monocyte motility. Upon eliminating the concentration gradient of 2-AG, the motility of the cells from the upper to lower compartment was sharply reduced, but not completely abrogated. This suggested that the chemotactic effect may not fully explain the observed change in cell migration. Of note, treatment of monocytes with 2-AG resulted in an enhanced secretion of the chemokines MCP-1 and IL-8. Moreover, exposure of the cells to 2-AG inhibited their migration towards MCP-1, while exposure to MCP-1 did not alter migration toward 2-AG. Taken together, our findings demonstrate that intracellular signaling cascades as well as induction of chemokine secretion contribute to the cannabinoid-mediated migration of monocytes.
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Dissertations / Theses on the topic "Monocytes – immunologie"

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Toufik, Jamila. "Interactions de copolymères fonctionnels dérivés du Sephadex avec le système du complément et les monocytes humains." Paris 13, 1994. http://www.theses.fr/1994PA132010.

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Chez les patients en état d'insuffisance rénale, les membranes d'hémodialyse à base de cellulose activent le système du complément et induisent la production d'interleukine-1 (il-1) par les monocytes. Le sephadex (seph) a été utilisé comme modèle de la cellulose. C'est un activateur du complément par la voie alterne; cette activation dépend de la présence d'anticorps anti-dextrane et de la surface de contact. Les carboxymethyle seph (cmseph) sont des inhibiteurs de cette activation. Les dérivés de seph: cmseph, cmbseph portant des groupes cmbenzylamide, cmbso3seph portant des groupes cmbsulfonates et deaeseph portant des groupes diethylaminoethyle, substitués à des taux variables, ont été choisis comme surfaces polysaccharidiques modèles d'étude de l'activation et de l'inhibition du complément et de l'induction de la production et de la sécrétion d'il-1par les monocytes humains. Les dosages hémolytiques ch50, radioimmunologiques de c3a et immuno-electrophoretiques de c3 ont montré que les cmbseph et cmbso3seph sont des activateurs du complément. Les deaeseph sont des inhibiteurs; cet effet est du au moins en partie au fait que les anticorps anti-dextranes ne reconnaissent plus les deaeseph. Après contact de tous ces dérivés avec des monocytes humains en absence de sérum, et en présence ou non de stimulateur microbien (lps), les dosages elisa d'il-1 intra et extracellulaires, montrent que seph et cmseph n'ont pas d'effet sur la production et la sécrétion d'il-1, cmbs03seph et surtout cmbseph stimulent la sécrétion, et surtout la production d'il-1 par les monocytes, deaeseph inhibe cette production.
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Bonnefont-Rebeix, Catherine. "Obtention et caractérisation de cellules dendritiques canines issues de monocytes." Lyon 1, 2006. http://www.theses.fr/2006LYO10292.

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Les cellules dendritiques (DC) sont largement étudiées chez l’homme et dans d’autres espèces animales, du fait de leur rôle central dans la régulation du système immunitaire. Leur forte capacité à présenter l’antigène a conduit à leur utilisation en immunothérapie vaccinale anti-tumorale. Le chien étant un très bon modèle dans les maladies auto-immunes, les greffes et les cancers, une meilleure caractérisation des DC canines (cDC) serait utile. Dans la première partie de ce travail, les cDC issues de monocytes (cMo-DC) et obtenues avec les facteurs de croissance cGM-CSF et cIL-4 expriment la molécule de costimulation CD86, spécifiquement induite par l’IL-4 canine (cIL-4), et le blocage du CD86 entraîne une inhibition de la prolifération induite par les cMo-DC en MLR. Dans la seconde partie, l’expression du TLR3 est explorée, ce récepteur étant fonctionnellement important et plus spécifiquement présent sur les DC humaines. Il s’avère que seules les cMo-DC montrent une forte expression intracellulaire du TLR3, comparativement aux autres leucocytes. Ainsi, étant donné le manque de marqueurs canins spécifiques, ce travail contribue à une meilleure caractérisation des cMo-DC, pouvant aider à leur utilisation en immunothérapie
Dentritic cells (DC) are widely investigated in human and many species, since they play a key role in the regulation of the immune system with their unique capacity of priming naïve T cells. Their high potency in antigen presentation has led several investigators to use them as vaccine adjuvants in therapy against tumors. Since dog is considered as a very interesting model in immune-mediated diseases, grafts and cancers, a better characterization of canine DC (cDC) is required. In the first part of this study, the expression of the costimulatory molecule CD86 was shown to be induced specifically by canine IL-4 on canine monocyte-derived DC (cMo-DC) in the presence of cGM-CSF plus cIL-4. The blocking of this CD86 led to the inhibition of cMo-DC-induced proliferation in MLR. The second part investigated the TLR3, a member of functionally important receptors family found to be more specifically expressed in human DC. TLR3 expression was strongly revealed at intracellular level in cMo-DC in comparison with other white blood cells. Therefore, since there is a lack of canine specific markers, these results contribute to a better characterization of cMo-DC, and may help for their use in immunotherapy
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Miranda, de Carvalho Camila. "Génération in vitro et caractérisation immunophénotypique des cellules dendritiques canines obtenues à partir de monocytes." Lyon 1, 2004. http://www.theses.fr/2004LYO10208.

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Actuellement, les cellules dendritiques (DCs) sont très étudiées chez l'homme et chez la souris. Cependant, les travaux expérimentaux restent assez pauvre pour la majorité des autres espèces animales. Le chien présente des pathologies cancéreuses et auto-immunes spontanées comparables à celles de l'homme. De ce fait, il paraît être un bon modèle animal potentiel pour évaluer la validité de l'immunomodulation par l'intermédiaire des cellules dendritiques. Dans un premier temps, nous avons développé une méthode visant à purifier les monocytes canins. Dans ce travail, nous avons pu mettre au point une méthode de purification des monocytes canins en combinant une technique d'élutriation et d'immunopurification complémentaire par des billes magnétiques. Ensuite, nous avons produit et caractérisé des Mo-DCs en utilisant de l'IL-4 et du GM-CSF de chien. Nous avons établi que la molécule CD86 était un marqueur spécifique de ces cellules dans cette espèce. Ces cellules dendritiques canines sont très fortement stimulantes en MLR et expriment aussi de façon importante les molécules CMH de Classe II et le CD32. Le marquage spécifique CD86 permettra de mieux purifier et analyser les fonctions de ces cellules chez le chien. Ces travaux permettrons de mieux caractériser et produire des cellules dendritiques canines pour envisager leur utilisation en immunothérapie et ouvrir les perspectives de recherche thérapeutiques chez cette espèce
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Nicolas-Gaulard, Isabelle. "Activité immunomodulatrice d'une protéine, l'hypodermine A, sur les cellules sanguines mononucléées des bovins." Paris 12, 1995. http://www.theses.fr/1995PA120031.

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Parmi les grandes maladies parasitaires qui affectent le cheptel bovin francais, l'hypodermose est responsable de pertes economiques importantes. Le premier stade larvaire de l'insecte responsable de cette parasitose provoque une desorganisation des systemes de defense de l'hote. Ces defaillances sont causees par les secretions larvaires et principalement par l'hypodermine a (ha). L'objet de ces travaux est l'etude de l'activite immunomodulatrice de l'ha sur les cellules sanguines mononucleees des bovins. L'ha inhibe la proliferation des lymphocytes apres stimulation par une lectine mitogene ou par un agent chimique et agit sur la phase precoce de l'activation cellulaire. De plus, l'indometacine, qui inhibe la synthese des prostaglandines, restaure la reponse proliferative des pbmc. La production en pge#2 est augmentee par l'ha dans les cultures de pbmc ou de monocytes. Les concentrations en pge#2 equivalentes a celles dosees dans les cultures en presence d'ha sont inhibitrices de la reponse proliferative a la phytohaemagglutinine. L'ha agirait donc sur la diminution de la reponse des pbmc par une voie dependante des prostaglandines. L'ha induit une baisse de la production d'il2 et beaucoup moins importante de l'ifn dans ces cultures stimulees par la phytohaemagglutinine. Une restauration de la proliferation des lymphocytes est observee par adjonction de surnageant enrichi en il2. La fonction accessoire des monocytes et la production de no, qui sont impliquees dans la proliferation des lymphocytes, sont inhibees par l'ha. L'ha module egalement l'expression de differents marqueurs a leur surface. Tous ces mecanismes decrits in vitro pourraient expliquer les phenomenes d'echappement du parasite au systeme immunitaire du bovin
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Baudesson, de Chanville Camille. "Rôle des monocytes dans la régulation de la réponse inflammatoire au cours du sepsis." Electronic Thesis or Diss., Sorbonne université, 2018. http://www.theses.fr/2018SORUS376.

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Le sepsis est une pathologie fréquente et grave. Il est défini comme un dysfonctionnement organique causé par une réponse dérégulée de l’hôte envers une infection. Une phase hyperinflammatoire précoce fait suite à la reconnaissance de l’agent pathogène et est progressivement remplacée par une immunosuppression à long terme entrainant une sensibilité prolongée des patients aux infections nosocomiales. Nos travaux ont montré que les Mo inflammatoires étaient fortement impliqués dans le contrôle de l’inflammation durant les phases précoces et tardives au cours d’un sepsis polymicrobien murin. En effet, lors de la phase « hyper-aiguë » la mobilisation des Mo participe à la surveillance et à la protection des tissus rénaux grâce à des mécanismes d’adhésion cellulaire dépendant du récepteur CX3CR1. La seconde phase du sepsis est le plus souvent décrite comme « immunosuppressive ». Nous avons mis en évidence une accumulation systémique des Mo et des PMN durant cette dernière phase. La caractérisation de leur localisation a montré que ces cellules s’accumulaient spécifiquement dans le réseau vasculaire des organes sans infiltrer les tissus. Les Mo Ly6Chigh et leurs récepteurs aux chimiokines CCR2 et CX3CR1 ont été identifiés comme essentiels à la surveillance pulmonaire lors d’une infection secondaire au sepsis. Cependant, la capacité de ces cellules à stimuler et à réguler les réponses immunitaires semble être altérée. Ainsi, l’état d’activation des Mo inflammatoires ne permettrait pas une protection efficace contre les infections opportunistes pulmonaires secondaires au sepsis
Sepsis is a common and life-threatening pathology. It is defined as an organic dysfunction caused by a dysregulated host response to infection. An initial hyper-inflammatory phase follows recognition of the pathogen and is progressively replaced by long-term immunosuppression leading to prolonged sensitivity to superinfections. Monocytes (Mo) are one of the first lines of phagocytic cells in the lung. Understanding how these cells participate in pulmonary supervision during sepsis would allow the development or improvement of treatments for enhancing resistance to secondary nosocomial infections. We showed that monocytes are strongly involved in the control of inflammation during the early and late phases of murine polymicrobial sepsis. Indeed, during the acute phase of sepsis, inflammatory monocyte mobilization participates to the monitoring of renal tissues and has a protective effect via a CX3CR1-dependent adhesion mechanism. The second phase of sepsis is most often described as “immunosuppressive”. We demonstrated a systemic accumulation of myeloid cells during this last phase. Characterization of their localization showed that these cells accumulated specifically in the vascular network of the organs without infiltrating the tissues. Ly6Chigh monocytes and their chemokine receptors CCR2 and CX3CR1 have been identified as essential for pulmonary supervision during first and second infection. However, the ability of these cells to stimulate and regulate immune responses appears to be impaired. Thus, the activation state of inflammatory Mo would not protect against a second pulmonary infections post sepsis
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Menasria, Rafik. "Caractérisation de la réponse immunitaire innée médiée par les monocytes/macrophages dans un modéle murin d'encéphalite herpétique." Thesis, Université Laval, 2013. http://www.theses.ulaval.ca/2013/29754/29754.pdf.

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Faivre, Valérie. "Régulation immunitaire au cours du sepsis altérations monocytaires et différenciation en sous populations de cellules dendritiques." Paris 7, 2007. http://www.theses.fr/2007PA077233.

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Le sepsis est une pathologie fréquente en réanimation. La mortalité est encore proche de 50% (cas les plus sévères). Il met en jeu une réaction pro- et anti-inflammatoire systémique, consécutive à une infection. Le rôle du système immunitaire est majeur, avec évolution possible vers un excès inflammatoire nocif mettant en danger les organes à distance du foyer infectieux, ou vers une réponse anti-inflammatoire trop intense favorisant les surinfections. Le but de ce travail a été de préciser les mécanismes de cette susceptibilité à l'infection, en particulier au niveau du monocyte. Les résultats montrent que les monocytes de patients (péritonite) sont capables de se différencier in vitro, et de façon accélérée, en cellule dendritique (DC). Dans ces DC, une sous population CD la- apparaît, en proportion très augmentée chez les patients. Des cellules T stimulées par des DC CD 1a- de donneurs contrôles ou de patients ne prolifèrent pas. Par contre, les DC CD 1a- contrôles induisent une polarisation Th2 et régulatrice, alors qu'avec les DC CD 1a- des patients l'orientation est plutôt Th1. Ceci pourrait favoriser la lutte contre l'infection mais aussi la destruction tissulaire des organes à distance. A l'inverse, les DC CD1a+ des patients semblent induire, avec une augmentation d'expression de FoxP3 dans les T en prolifération, un profil régulateur plus fort que les DC CD1a+ contrôles. Ces résultats suggèrent l'existence d'un contrôle de la réponse inflammatoire et immunitaire au cours du sepsis par l'apparition de populations monocytaires à définir, suite à un processus durable de reprogrammation cellulaire. La participation de ce processus dans les surinfections est à préciser
Sepsis is frequently observed in intensive care, with mortality around 50% (most severe cases). This pathology involves a systemic inflammatory response that occurs following infection. The immune System plays a major role in this inflammatory syndrome, with a potential progression toward an excessive response, dangerous for peripheral organs, or toward inadequate anti-inflammatory control and re-infections. The aim of this work was to precise mechanisms involved in this infection susceptibility, especially those related to monocyte. Results showed that peritonitis patients monocytes are able to differerentiate in vitro into dendritic cells (DC), in an accelerated manner. Ànalysis of these DC showed the emergence of a CD la- DC subset, which proportion is strongly increased in patients. T cells stimulated with control donors or patients CD la- DC do not proliferate. However, T cells cultured with control CD la- DC display Th2 and regulatory polarization, whereas patients CD la- DC favored Th1 profile. This polarization switch could enhance immune response against infection, but also peripheral tissue injury. By contrast, patients CDla+ DC potentially induced a stronger regulatory response in proliferating T cells, as suggested by increased Foxp3 expression, than did control CDla+ cells. These results suggest an additionnal and complex control of inflammatory and immune responses during sepsis, that could take place via the development of monocytes subsets, which remains to be characterized, and could result from a long-lasting cellular reprogramming process. The involvement of this process in the occurrence of secondary infections needs further investigations
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García, Téllez Thalia Alejandra. "Study of inflammasome activation in monocytes, macrophages and epithelial cells during SIV infection in a pathogenic and a non-pathogenic model." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC300.

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Chez les individus infectés par le VIH on observe une augmentation de l’inflammation et de l’activation immunitaire (AI) qui est associée à la progression vers le SIDA. Même en présence de traitements antirétroviraux, les niveaux d’AI restent élevés et sont associés à une morbidité et une mortalité accrues. Les mécanismes moléculaires derrière l’AI ne sont pas bien caractérisés. L’activation des macrophages (Mφ ) et monocytes et la translocation bactérienne peuvent jouer un rôle important. Contraire aux humains, et au model pathogène de l’infection (macaques, MAC), les hôtes naturels du SIV (Singes vertes d’Afrique, AGM), résoudraient l’inflammation aiguë, ils montrent un niveau plus bas de cytokines inflammatoires comme l’IL-1β et l’IL-18 et l’IA chronique est absente. L’IL-1β et l’IL-18 sont produits par le Mφ et les cellules épithéliales de l’intestine (IEC) auprès l’activation de l’inflammasome. Nous avons étudié l’activation de l’inflammasome chez les hôtes naturels, dans quel tissues ceci peut avoir lieu et s’il existe des différences entre les deux modelés d’infection. Pour cela, nous avons mesuré les niveaux plasmatiques de l’IL-1β et l’IL-18 au cours de l’infection ; nous avons analysé le marquage des Mφ , IEC et IL-18 par microscopie confocale; nous avons mis en place des essaies fonctionnels pour l’activation in vitro de l’inflammasome et nous avons développé les outils pour le phenotypage et l’isolation de Mφ et IEC du sang, du poumon, du LAB, des ganglions et de l’intestine. Nous avons montré que l’inflammasome est activé lors de l’infection par SIV dans les modèles pathogène et non-pathogène, en particulier dans l’intestine grêle. Notre étude indique une production plus notable d’IL-18 dans le jéjunum des MAC infectés en comparaison avec des AGM. Nous avons montré que l’inflammasome peut être activé dans les macrophages par des signaux de l’environnement présent lors de la translocation bactérienne et le stress cellulaire, comme le LPS et l’ATP. Nous avons montré de différences au niveau de régulation de la réponse liée à l’inflammasome. Les niveaux d’IL-18BP et l’IL-1RA, les antagonistes de l’IL-18 et l’IL-1β respectivement, sont été plus élevés chez les AGM que chez les MAC. On a trouvé une corrélation entre les niveaux de IL-18BP/IL-1Ra et les niveaux plasmatiques des agonistes chez les hôtes naturelles mais pas chez les MAC, ce qui est indicative de une régulation potentiellement plus efficace chez les AGM
Chronic immune activation drives progression toward AIDS in HIV infection and still remains in low levels in antiretroviral-treated patients increasing the risk of non-communicable diseases. Such non-AIDS co-mobility and mortality is associated with markers of monocyte/macrophage (Mφ ) activation and microbial translocation, but the molecular bases of this phenomenon remain unknown. In contrast to humans and pathogenic animal models of HIV (i.e. macaques, MAC), natural hosts of SIV (i.e. African Green Monkeys, AGM) quickly resolve SIV-induced inflammation and display lower levels of IL-1β and IL-18. IL-1β and IL-18 can be produced by Mφ or intestinal epithelial cells (IEC) upon inflammasome activation with potential multiple roles. Therefore, we studied whether the inflammasome activation upon SIV-infection occurs in natural hosts, in which tissues it might take place and if it differs between models. To do so, we measured plasmatic IL-1β and IL-18 levels along SIV-infection; we performed microscopy staining of Mφ , IEC and IL-18 in tissues, we set-up functional assays for inflammasome activation in-vitro and we developed tools for phenotyping and isolating Mφ and IEC from blood, lung, BAL, LN and gut. We showed inflammasome activation in vivo during pathogenic and non-pathogenic SIV infection evaluated by IL-18 in the gut of MAC and AGM, particularly in the small intestine, as well as by the levels of IL-18 and IL-1β in plasma. Our study indicated higher IL-18 production in the jejunum of SIV-infected MAC as compared to SIV-infected AGM. We showed that signals that might be in the environment during pathogenic SIVmac infection, in particular LPS and ATP as a result of microbial translocation and stress activate the inflammasome of MAC and AGM macrophages. We revealed differences at the level of the regulation between both models, observed by higher levels of IL-18BP and IL-1RA in AGM compared to MAC and correlations between IL-18, IL-1β and their respective antagonists only in AGM but not in MAC
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Le, Pan Yanaëlle. "Étude de la biocompatibilité des surfaces artificielles au cours de l'hémodialyse." Compiègne, 1998. http://www.theses.fr/1998COMP1105.

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Nous avons étudié, in vitro et in vivo, si le complément et l'activation des leucocytes chez des patients dialysés étaient directement liés. Nous avons montré que les anaphylatoxines induisent la production de cytokines proinflammatoires et préférentiellement MCP-1. De plus, la sécrétion d'IL-1 et de son antagoniste naturel est dans un rapport ne contrebalançant pas les effets biologiques de l'IL-l. Dans un protocole clinique, 6 patients ont été dialysés chacun sur 3 types de membranes activant le complément à divers degrés. Nous avons mesuré l'activation du complément, l'expression des molécules d'adhérence, la leucopénie, la production de cytokines et les gaz du sang. Le nombre de neutrophiles et de monocytes diminue après 5 et 15 minutes de dialyse en fonction du type de membrane utilisée. Cette margination ne corrélait pas avec l'activation du complément sauf chez les dialysés sur la membrane la moins activatrice du complément. Un pourcentage important de cellules contenant des cytokines proinflammatoires (IL-1 , IL-1 , IL-8, TN) chez les patients dialysés avec la cuprophane a été détecté. Les cellules qui stockent de l'IL-1 ne produisent pas toutes de l'IL-lra et peuvent donc avoir in vivo un potentiel proinflammatoire. En accord avec d'autres études, nous suggérons que d'autres facteurs que le C3a interviendraient dans l'augmentation de l'expression membranaire de C11 b sur les neutrophiles. Nous n'avons trouvé aucune corrélation entre l'expression des molécules d'adhérence membranaires ou solubles et l'activation du complément, entre l'expression des molécules d'adhérence solubles et membranaires, entre les variations des pO2 et pCO2 et l'activation du complément. Contrairement à d'autres études nous n'avons pas trouvé de lien entre le nombre de cellules circulantes et l'activation du complément. L'activation du complément n'est donc pas en relation directe avec la modulation des paramètres immunologiques, que nous avons étudiés, au cours de la dialyse.
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Hastir, Jean-Francois. "Study of the fate of resident macrophages and monocytes upon partial liver resection and their impact on hepatocarcinoma outgrowth." Doctoral thesis, Universite Libre de Bruxelles, 2020. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/308316.

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Partial hepatectomy (PH) is a treatment of choice for patients suffering from early stage hepatocellular carcinoma (HCC). Ablation of large proportion of the liver is rendered possible because of the ability of the liver to regenerate. Yet, a significant number of patients will experience recursion of the disease. Such relapses are unfortunately rather frequent and constitute a bad prognosis. The development of new strategies aiming at reducing the risk of recursion of HCC is thus a paramount element of the surgery-based treatment. Some previous studies have proposed that the regenerative process as well as the fate of the immune cells during the liver regeneration process is linked to this recurrence phenomenon.In this study, we investigated the impact of PH on HCC development in a pre-clinical murine model. We implanted Hepa1-6 hepatocarcinoma cells (a murine hepatocarcinoma cell line) directly in the liver of mice and compared a non-resected group with a group undergoing 40% PH one week following tumor implantation. Analysis were relying on bioluminescence imaging and flow cytometry. We demonstrated that liver regeneration increases tumoral proliferation. This proliferation was associated with a reduction in the number of liver resident macrophages, i.e. Kupffer cells (KC). KC anti-tumoral activity was also proved using conditional ablation model. We further studied the mechanisms leading to this disappearance and demonstrated that, under normal regeneration conditions, PH-induced KC number reduction was dependent on tumor necrosis factor-α (TNF-α), receptor interacting protein kinase (RIPK) 3 and caspase-8 activation whereas interleukin (IL)-6 acted as a KC pro- survival signal. In mice with previous Hepa 1-6 encounter, the KC reduction changed toward a TNF-α-RIPK3-caspase-1 activation. This data suggest a switch from apoptosis to pyroptosis induction in KC following PH. Moreover, KC disappearance associated with caspase-1 activity induced the recruitment of monocyte derived cells that are beneficial for tumor growth while caspase-8 dependent reduction did not, underlying the importance of macrophages activated death-pathway in regulating the anti-tumoral immune response. Our results show the necessity for comprehensive multidisciplinary treatment approach following PH and propose new targets in order to reduce the relapse of the disease occurring after surgery.
Doctorat en Sciences biomédicales et pharmaceutiques (Médecine)
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Books on the topic "Monocytes – immunologie"

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M, Zembala, and Asherson G. L, eds. Human monocytes. London: Academic, 1989.

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van, Furth Ralph, ed. Hemopoietic growth factors and mononuclear phagocytes. Basel: New York, 1993.

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Book chapters on the topic "Monocytes – immunologie"

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Gu, L., S. C. Tseng, and B. J. Rollins. "Monocyte Chemoattractant Protein-1." In Chemical Immunology and Allergy, 7–29. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000058723.

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Gershwin, Laurel J. "Case 31: Monocytic Ehrlichiosis." In Case Studies in Veterinary Immunology, 151–55. New York, NY : Garland Science, [2017]: Garland Science, 2017. http://dx.doi.org/10.4324/9781315165462-31.

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Sugden, Scott, Damien Montamat-Sicotte, Karen K. Yam, Joseph Murphy, Bader Yassine Diab, and Virginia Litwin. "Monocyte and lymphocyte membrane markers: Ontogeny and clinical significance." In Medical Immunology, 115–39. 7th edition. | Boca Raton : Taylor & Francis, 2020.: CRC Press, 2019. http://dx.doi.org/10.1201/9780429278990-10.

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Beeken, W., J. Fabian, D. Meyer, and D. Gump. "Human colon epithelial cell lysates evoke monocyte chemotaxis." In Advances in Mucosal Immunology, 44–45. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_9.

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Larsson, L. G., F. Bahram, S. Wu, F. Öberg, K. Nilsson, and B. Lüscher. "Cytokine-induced Inhibition of Myc Activity in Monocytic Cells." In Current Topics in Microbiology and Immunology, 191–200. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60801-8_19.

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Eccles, Michael R., William R. Baumbach, Gregory D. Schuler, and Michael D. Cole. "Studies of Secondary Transforming Events in Murine c-myc Retrovirus-Induced Monocyte Tumors." In Current Topics in Microbiology and Immunology, 89–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74623-9_8.

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Freundlich, B., N. Sandorfi, C. Altman, and J. Tomaszewski. "Monocyte/Macrophage Infiltrates in the Salivary Glands of Women with Silicone Breast Implants." In Current Topics in Microbiology and Immunology, 323–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-85226-8_34.

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Vassalli, J. D., A. Wohlwend, and D. Belin. "Urokinase-Catalyzed Plasminogen Activation at the Monocyte/Macrophage Cell Surface: A Localized and Regulated Proteolytic System." In Current Topics in Microbiology and Immunology, 65–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77377-8_3.

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Mózes, T., T. Mészáros, J. Wille, and G. Berentey. "The Relationship Between Platelet, Lymphocyte and Monocyte Counts, Sepsis and Survival in Polytrauma Patients." In Immunology and Its Impact on Infections in Surgery, 187–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79079-9_26.

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Baumbach, William R., E. Richard Stanley, and Michael D. Cole. "Induction of Clonal Monocyte/Macrophage Tumors in vivo by a Mouse c-myc Retrovirus: Evidence for Secondary Transforming Events." In Current Topics in Microbiology and Immunology, 23–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71562-4_4.

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Conference papers on the topic "Monocytes – immunologie"

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Altieri, Dario C., Rossella Bader, and Pier M. Mannucci. "STRUCTURAL DIVERSITY AMONG CELLULAR ADHESION RECEPTORS: FIBRINOGEN BINDING IS A NOVEL BIOLOGICAL PROPERTY OF THE MONOCYTE DIFFERENTIATION ANTIGEN OKM1." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643851.

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A family of related glycoproteins (GP) mediate the interaction between the circulating adhesive proteins and a variety of cells (cytyoadhesins). In this study we have compared two cell-surface antigens which share the property to bind fibrinogen: the platelet GP IIb/IIIa, prototype of the cytoadhesins, and the receptor for fibrinogen costitutively synthesized by monocytes. Two anti-GP IIb/IIIa monoclonal antibodies (Mabs) (LJP9, LJP5), recognizing functionally distinct epitopes of the GP IIb/IIIa did not react with monocytes nor inhibited 125I-fibrinogen binding to monocytes. Similarly, an Arg-Gly-Asp containing peptide which completely abolished platelet-fibrinogen interaction, had no effect on monocytes. Structurally, the monocyte fibrinogen receptor was dimeric and composed of two subunits with molecular weight (Mr) of 155,000 and 95,000. This structural organization was different from that of the GP IIb/IIIa (Mr= 116,000), but in close analogy with the family of leukocyte differentiation antigens OKM1, LFA-1. Therefore, this possible relationship was investigated. A Mab to OKM1 antigen (10 μg/ml) completely suppressed fibrinogen binding to monocytes while it was ineffective on plateles. Iodinated monocyte lysate subjected to immunoprecipitation with OKM1 Mab (60 μg/ml) showed a dimeric antigen with the same molecular size of the monocyte fibrinogen receptor. Moreover, preclearing of the monocyte lysate with OKM1 Mab removed the immunoprecipitate corresponding to the monocyte fibrinogen receptor. These data indicate that the immunologic differentiation antigen OKM1, in addition to function as a complement receptor, displays also the novel biological adhesion property to mediate the binding of fibrinogen to monocytes.
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Connolly, Kelli, David Linehan, and Scott Gerber. "Abstract B01: Enhancing radiotherapy by targeting inflammatory monocytes." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-b01.

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Sanford, Dominic E., Brian A. Belt, Roheena Z. Panni, Jonathan B. Mitchem, David G. Denardo, S. Peter Goedegebuure, and David C. Linehan. "Abstract A64: Peripheral blood monocytes predict survival in pancreatic cancer." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a64.

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Boussommier-Calleja, Alexandra, and Roger Kamm. "Abstract B22: Role of monocytes in 3D microfluidic models of cancer cell extravasation." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-b22.

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Kim, Hyun-Jin. "Abstract PO012: A subset of monocyte-derived macrophages in glioblastoma multiforme supports antitumor immune responses." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po012.

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Beckman, Michael J., Michael Cavnar, Adrian Seifert, Juan Santamaria-Barria, Jennifer Zhang, Adam Levy, Ferdinand Rossi, Shan Zeng, and Ronald P. DeMatteo. "Abstract B64: CSF1R-dependent tumor-associated macrophages arise from bone marrow-derived monocytes and promote gastrointestinal stromal tumor development." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b64.

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Singh, Latika, Peter Stivers, Anthony Palmieri, Mark Zhang, Barbara Joyce-Shaikh, Jie Zhang-Hoover, Yujie Qu, Alan Byford, Michael Meehl, and Philip Brandish. "Abstract B84: In vitro and in vivo characterization of tumor-educated human monocytic myeloid-derived suppressor cells." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b84.

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Xiang, Handan, Carlo Ramil, Josephine Hai, Chunsheng Zhang, Huijun Wang, Amanda A. Watkins, Roshi Afshar, et al. "Abstract A98: Cancer-associated fibroblasts promote immunosuppression by inducing NOX2-expressing monocytic MDSCs in lung squamous cell carcinoma." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a98.

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Wilski, Nicole A., Christina Del Casale, Vitali Alexeev, Constantine Daskalakis, Timothy J. Purwin, Andrew E. Aplin, and Christopher M. Snyder. "Abstract A74: Cytomegalovirus infection of melanoma delays tumor growth by recruiting and altering monocytic phagocytes in the tumor." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a74.

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Zelante, Bruna, and José Alexandre Marzagão Barbuto. "Abstract A84: Altered monocyte-derived dendritic cell differentiation in the presence of tumor supernatant: Possible involvement the p38MAPK pathway." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a84.

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