Bibliografie tematiche / Macrophage inhibitory cytokine

Letteratura scientifica selezionata sul tema "Macrophage inhibitory cytokine"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 1 febbraio 2022

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Articoli di riviste sul tema "Macrophage inhibitory cytokine"

1

Colon-Echevarria, Claudia B., Tatiana Ortiz, Lizette Maldonado, Melanie J. Hidalgo-Vargas, Jaileene Pérez-Morales, Alexandra N. Aquino-Acevedo, Roberto Herrera-Noriega, Margarita Bonilla-Claudio, Eida M. Castro e Guillermo N. Armaiz-Pena. "Zoledronic Acid Abrogates Restraint Stress-Induced Macrophage Infiltration, PDGF-AA Expression, and Ovarian Cancer Growth". Cancers 12, n. 9 (18 settembre 2020): 2671. http://dx.doi.org/10.3390/cancers12092671.

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Multiple studies suggest that chronic stress accelerates the growth of existing tumors by activating the sympathetic nervous system. Data suggest that sustained adrenergic signaling can induce tumor growth, secretion of pro-inflammatory cytokines, and macrophage infiltration. Our goal was to study the role of adrenergic-stimulated macrophages in ovarian cancer biology. Cytokine arrays were used to assess the effect of adrenergic stimulation in pro-tumoral cytokine networks. An orthotopic model of ovarian cancer was used to assess the in vivo effect of daily restraint stress on tumor growth and adrenergic-induced macrophages. Cytokine analyses showed that adrenergic stimulation modulated pro-inflammatory cytokine secretion in a SKOV3ip1 ovarian cancer cell/U937 macrophage co-culture system. Among these, platelet-derived growth factor AA (PDGF-AA), epithelial cell-derived neutrophil-activating peptide (ENA-78), Angiogenin, vascular endothelial growth factor (VEGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-5 (IL-5), Lipocalin-2, macrophage migration inhibitory factor (MIF), and transferrin receptor (TfR) were upregulated. Enriched biological processes included cytokine-mediated signaling pathways and positive regulation of cell proliferation. In addition, daily restraint stress increased ovarian cancer growth, infiltration of CD68+ macrophages, and expression of PDGF-AA in orthotopic models of ovarian cancer (SKOV3ip1 and HeyT30), while zoledronic acid, a macrophage-depleting agent, abrogated this effect. Furthermore, in ovarian cancer patients, high PDGFA expression correlated with worse outcomes. Here, it is shown that the adrenergic regulation of macrophages and PDGFA might play a role in ovarian cancer progression.
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2

Lu, Chunxia, P. Anil Kumar, Yong Fan, Mark A. Sperling e Ram K. Menon. "A Novel Effect of Growth Hormone on Macrophage Modulates Macrophage-Dependent Adipocyte Differentiation". Endocrinology 151, n. 5 (25 febbraio 2010): 2189–99. http://dx.doi.org/10.1210/en.2009-1194.

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The GH receptor (GHR) is expressed on macrophages. However, the precise role of GH in regulation of macrophage function is unclear. We hypothesized that soluble factors including cytokines produced by macrophages in a GH-dependent manner regulate adipogenesis. We confirmed expression and functional integrity of the GHR in the J774A.1 macrophage cells. Conditioned medium (CM) from macrophages inhibited adipogenesis in a 3T3-L1 adipogenesis assay. CM from GH-treated macrophages decreased the inhibitory effect of CM from macrophages on adipogenesis. This effect on preadipocyte differentiation was active only during the first (early) phase of adipocyte differentiation. CM from stromal vascular compartment macrophages of mice with macrophage-specific deletion of the GHR exhibited more inhibitory effect on 3T3-L1 preadipocyte differentiation compared with CM from stromal vascular compartment macrophages of control mice, indicating that intact GH action in primary macrophages also increases preadipocyte differentiation. GH did not increase IGF-1 expression in macrophages. PCR array analysis identified IL-1β as a candidate cytokine whose expression was altered by GH in macrophages. Levels of IL-1β mRNA and protein were significantly decreased in GH-treated J774A.1 macrophages. Nuclear factor-κB stimulates IL-1β gene expression, and GH induced a significant decrease in the levels of phosphorylated nuclear factor-κB in macrophages. IL-1β is a known inhibitor of adipogenesis, and these results support GH-dependent down-regulation of macrophage IL-1β expression as one mechanism for the observed increase in adipogenesis with CM from GH-treated macrophages. We conclude that GH decreases secretion of IL-1β by the macrophage and thus in a paracrine manner increases adipocyte differentiation. These results provide a novel mechanism for GH’s actions in the control of adipogenesis.
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Borsini, Alessandra, Maria Grazia Di Benedetto, Juliette Giacobbe e Carmine M. Pariante. "Pro- and Anti-Inflammatory Properties of Interleukin in Vitro: Relevance for Major Depression and Human Hippocampal Neurogenesis". International Journal of Neuropsychopharmacology 23, n. 11 (29 luglio 2020): 738–50. http://dx.doi.org/10.1093/ijnp/pyaa055.

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Abstract Background Although the pro-inflammatory cytokine interleukin (IL)6 has been generally regarded as “depressogenic,” recent research has started to question this assumption in light of the fact that this cytokine can also have anti-inflammatory properties. This bimodal action seems to be dependent on its concentration levels and on the concomitant presence of other pro-inflammatory cytokines. Methods We exposed a human hippocampal progenitor cell line, HPC0A07/03C, to cytokine levels described in depressed patients (IL6 5 pg/mL with IL1β 10 pg/mL or Macrophage Migration Inhibitory Factor (300 pg/mL) in healthy individuals (IL6 with IL1β, 1 pg/mL or Macrophage Migration Inhibitory Factor 10 pg/mL), as well as to the potentially anti-inflammatory, much higher concentrations of IL6 (50 000 pg/mL). Results Treatment with high concentrations of IL6 with IL1β or Macrophage Migration Inhibitory Factor (resembling depressed patients) decreases neurogenesis compared with low concentrations of the same cytokines (healthy individuals) and that this is mediated via production of, respectively, IL8 and IL1β in cell supernatant. Instead, treatment with very high, anti-inflammatory concentration of IL6 (50 000 pg/mL) together with high IL1β or Macrophage Migration Inhibitory Factor prevents decrease in neurogenesis and reduces both IL8 and IL1β. When high concentrations of both IL1β and Macrophage Migration Inhibitory Factor were used in co-treatment, as a model of treatment-resistant depression, we also demonstrated a reduction in neurogenesis and that this is mediated via a decrease in IL4; moreover, co-treatment with high IL1β and Macrophage Migration Inhibitory Factor and the very high concentration of IL6 prevented the reduction in neurogenesis and increased IL4. Conclusions Our results demonstrate that IL6 can exert both pro- and anti-inflammatory (potentially antidepressant) properties, depending on its concentrations and combinations with other inflammatory cytokines.
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Kasama, Tsuyoshi, Kumiko Ohtsuka, Michihito Sato, Ryo Takahashi, Kuninobu Wakabayashi e Kazuo Kobayashi. "Macrophage Migration Inhibitory Factor: A Multifunctional Cytokine in Rheumatic Diseases". Arthritis 2010 (3 gennaio 2010): 1–10. http://dx.doi.org/10.1155/2010/106202.

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Macrophage migration inhibitory factor (MIF) was originally identified in the culture medium of activated T lymphocytes as a soluble factor that inhibited the random migration of macrophages. MIF is now recognized to be a multipotent cytokine involved in the regulation of immune and inflammatory responses. Moreover, the pivotal nature of its involvement highlights the importance of MIF to the pathogenesis of various inflammatory disorders and suggests that blocking MIF may be a useful therapeutic strategy for treating these diseases. This paper discusses the function and expressional regulation of MIF in several rheumatic diseases and related conditions.
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Huh, Sung Jin, Chin-Ying Chung, Arati Sharma e Gavin P. Robertson. "Macrophage Inhibitory Cytokine-1 Regulates Melanoma Vascular Development". American Journal of Pathology 176, n. 6 (giugno 2010): 2948–57. http://dx.doi.org/10.2353/ajpath.2010.090963.

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6

Calandra, T., J. Bernhagen, R. A. Mitchell e R. Bucala. "The macrophage is an important and previously unrecognized source of macrophage migration inhibitory factor." Journal of Experimental Medicine 179, n. 6 (1 giugno 1994): 1895–902. http://dx.doi.org/10.1084/jem.179.6.1895.

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Abstract (sommario):
For over 25 years, the cytokine known as macrophage migration inhibitory factor (MIF) has been considered to be a product of activated T lymphocytes. We recently identified the murine homolog of human MIF as a protein secreted by the pituitary in response to endotoxin administration. In the course of these studies, we also detected MIF in acute sera obtained from endotoxin-treated, T cell-deficient (nude), and hypophysectomized mice, suggesting that still more cell types produce MIF. Here, we report that cells of the monocyte/macrophage lineage are an important source of MIF in vitro and in vivo. We observed high levels of both preformed MIF protein and MIF mRNA in resting, nonstimulated cells. In the murine macrophage cell line RAW 264.7, MIF secretion was induced by as little as 10 pg/ml of lipopolysaccharide (LPS), peaked at 1 ng/ml, and was undetectable at LPS concentrations > 1 microgram/ml. A similar stimulation profile was observed in LPS-treated peritoneal macrophages; however, higher LPS concentrations were necessary to induce peak MIF production unless cells had been preincubated with interferon gamma (IFN-gamma). In RAW 264.7 macrophages, MIF secretion also was induced by tumor necrosis factor alpha (TNF-alpha) and IFN-gamma, but not by interleukins 1 beta or 6. Of note, MIF-stimulated macrophages were observed to secrete bioactive TNF-alpha. Although previously overlooked, the macrophage is both an important source and an important target of MIF in vivo. The activation of both central (pituitary) and peripheral (macrophage) sources of MIF production by inflammatory stimuli provides further evidence for the critical role of this cytokine in the systemic response to tissue invasion.
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Baer, Mark, Allan Dillner, Richard C. Schwartz, Constance Sedon, Sergei Nedospasov e Peter F. Johnson. "Tumor Necrosis Factor Alpha Transcription in Macrophages Is Attenuated by an Autocrine Factor That Preferentially Induces NF-κB p50". Molecular and Cellular Biology 18, n. 10 (1 ottobre 1998): 5678–89. http://dx.doi.org/10.1128/mcb.18.10.5678.

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ABSTRACT Macrophages are a major source of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-α), which are expressed during conditions of inflammation, infection, or injury. We identified an activity secreted by a macrophage tumor cell line that negatively regulates bacterial lipopolysaccharide (LPS)-induced expression of TNF-α. This activity, termed TNF-α-inhibiting factor (TIF), suppressed the induction of TNF-α expression in macrophages, whereas induction of three other proinflammatory cytokines (interleukin-1β [IL-1β], IL-6, and monocyte chemoattractant protein 1) was accelerated or enhanced. A similar or identical inhibitory activity was secreted by IC-21 macrophages following LPS stimulation. Inhibition of TNF-α expression by macrophage conditioned medium was associated with selective induction of the NF-κB p50 subunit. Hyperinduction of p50 occurred with delayed kinetics in LPS-stimulated macrophages but not in fibroblasts. Overexpression of p50 blocked LPS-induced transcription from a TNF-α promoter reporter construct, showing that this transcription factor is an inhibitor of the TNF-α gene. Repression of the TNF-α promoter by TIF required a distal region that includes three NF-κB binding sites with preferential affinity for p50 homodimers. Thus, the selective repression of the TNF-α promoter by TIF may be explained by the specific binding of inhibitory p50 homodimers. We propose that TIF serves as a negative autocrine signal to attenuate TNF-α expression in activated macrophages. TIF is distinct from the known TNF-α-inhibiting factors IL-4, IL-10, and transforming growth factor β and may represent a novel cytokine.
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Bozza, Marcelo T., Yuri C. Martins, Letícia A. M. Carneiro e Claudia N. Paiva. "Macrophage Migration Inhibitory Factor in Protozoan Infections". Journal of Parasitology Research 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/413052.

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Abstract (sommario):
Macrophage migration inhibitory factor (MIF) is a cytokine that plays a central role in immune and inflammatory responses. In the present paper, we discussed the participation of MIF in the immune response to protozoan parasite infections. As a general trend, MIF participates in the control of parasite burden at the expense of promoting tissue damage due to increased inflammation.
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Nishi, Kosuke, Takako Ito, Ayumu Kadota, Momoko Ishida, Hisashi Nishiwaki, Naohiro Fukuda, Naoaki Kanamoto, Yoko Nagata e Takuya Sugahara. "Aqueous Extract from Leaves of Citrus unshiu Attenuates Lipopolysaccharide-Induced Inflammatory Responses in a Mouse Model of Systemic Inflammation". Plants 10, n. 8 (19 agosto 2021): 1708. http://dx.doi.org/10.3390/plants10081708.

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Inflammation is related to various life-threatening diseases including cancer, neurodegenerative diseases, and metabolic syndrome. Because macrophages are prominent inflammatory cells, regulation of macrophage activation is a key issue to control the onset of inflammation-associated diseases. In this study, we aimed to evaluate the potential anti-inflammatory activity of Citrus unshiu leaf extract (CLE) and to elucidate the mechanism underlying its anti-inflammatory effect. We found the inhibitory activity of CLE on the secretion of proinflammatory cytokines and a chemokine from mouse macrophage-like RAW 264.7 cells and mouse peritoneal macrophages. The inhibitory activity of CLE was attributed to downregulated JNK, p38 MAPK, and NF-κB signaling pathways, leading to suppressed gene expression of inflammation-associated proteins. Oral administration of CLE significantly decreased the serum level of proinflammatory cytokines IL-6 and TNFα and increased that of anti-inflammatory cytokine IL-10 in lipopolysaccharide-induced systemic inflammation mice. In addition, oral administration of CLE decreased secretion and gene expression of several proinflammatory proteins in the liver and spleen of the model mice. Overall results revealed that C. unshiu leaf is effective to attenuate inflammatory responses in vitro and in vivo.
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Lemay, Serge, Tatiana V. Lebedeva e Ajay K. Singh. "Inhibition of Cytokine Gene Expression by Sodium Salicylate in a Macrophage Cell Line through an NF-κB-Independent Mechanism". Clinical Diagnostic Laboratory Immunology 6, n. 4 (1 luglio 1999): 567–72. http://dx.doi.org/10.1128/cdli.6.4.567-572.1999.

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ABSTRACT Macrophage-derived cytokines and chemokines are involved at multiple steps of immune and inflammatory responses, and the transcriptional factor NF-κB appears to play a pivotal role in their coordinated upregulation. The anti-inflammatory agents salicylates have been proposed to act in part by inhibiting NF-κB. We have therefore studied the effects of sodium salicylate on lipopolysaccharide (LPS)-induced κB-binding activity and on cytokine and chemokine gene expression in the RAW264.7 murine macrophage cell line and compared them to those of an established NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC). PDTC (100 μM) completely abrogated LPS-induced κB-binding activity and also profoundly inhibited the induction of interleukin 1α (IL-1α), IL-1β, IL-6, IL-10, granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, and MCP-1 and, to a lesser extent, leukemia inhibitory factor, RANTES, and IL-1Ra. In contrast, sodium salicylate (15 to 20 mM) had no effect on NF-κB activation but, nevertheless, suppressed several LPS-induced cytokine and chemokine genes to a degree similar to that obtained with PDTC. However, compared to PDTC, sodium salicylate caused significantly less inhibition of IL-1Ra and IL-10 gene expression after LPS stimulation. Neither LPS-induced MIP-1α, MIP-1β, nor MIP-2 was significantly affected by PDTC or sodium salicylate, demonstrating that NF-κB is dispensable for the transcriptional regulation of these genes by LPS. In summary, these results suggest that both NF-κB-dependent and NF-κB-independent pathways are necessary for the induction by LPS of a complex cytokine and chemokine response. In the RAW264.7 macrophage cell line, suprapharmacological concentrations of sodium salicylate exert a potent inhibitory effect on LPS-induced cytokine gene induction but appear to accomplish this by interfering with NF-κB-independent pathways of activation.
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Più fonti

Tesi sul tema "Macrophage inhibitory cytokine"

1

Patrikainen, Lila. "Prostatic gene expression : probasin, human prostatic acid phosphatase and macrophage inhibitory cytokine-1 as model genes /". Oulu : Oulun yliopisto, 2004. http://herkules.oulu.fi/isbn9514272730/.

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Patrikainen, L. (Lila). "Prostatic gene expression: probasin, human prostatic acid phosphatase and macrophage inhibitory cytokine-1 as model genes". Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514272730.

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Abstract (sommario):
Abstract Gene products that are only expressed in one tissue or cell type are useful models for investigating the biochemical and molecular mechanisms of tissue/cell-specific gene regulation. The regulatory regions of such genes are also practical tools in gene therapy. In this work, prostate-specific and androgen-dependent gene regulation was investigated by using human prostatic acid phosphatase (hPAP) and rat probasin (rPB) as models. In DNase I footprinting, a protected 12 bp region was found in the PB gene between the nucleotides -251 and -240 only with nuclear extracts of prostatic origin. The sequence of this area was GAAAATATGATA. Weak interaction could be detected between the DNA-binding domain of AR and the prostatic transcription factor. The results also suggested that the prostatic regulatory protein makes AR binding to its response element more effective and concomitantly magnifies the effect of androgen. A hPAP construct containing the sequence between the nucleotides -734 and +467 in front of the CAT reporter gene was highly expressed in the prostate of transgenic mice. Five homologues (A-E) for our previously identified prostate-specific GAAAATATGATA DNA-binding site were found in the area where the sites C and E could bind the regulatory protein in EMSA. The prostatic transcription factor complex bound to the GAAAATATGATA site was purified and characterized from a suspension-adapted mass culture of PC-3 prostate cancer cells by using sequence-specific DNA affinity chromatography, mass spectrometry and supershifts. Several potential transcription factors were identified, but only USF2 was confirmed to be part of the transcription factor complex. Two PC-3 cell line variants (anchorage-dependent and suspension-adapted, anchorage-independent variants) were used as a model for advanced, androgen-independent prostate cancer. Genes that were overexpressed in a suspension-adapted PC-3 cell line were further investigated, since they can be considered as putative markers of metastatic activity. The macrophage inhibitory cytokine-1 (MIC-1) gene, which was overexpressed in the suspension-adapted PC-3 cell line, was further investigated in order to clarify the mechanism behind aggressive cell growth and androgen-independent gene regulation. In patient specimens, MIC-1 had no or low expression in benign prostatic hyperplasia and normal prostate but high in prostatic cancer and therefore it could be a useful marker for aggressive prostate cancer. Indomethacin increased the expression of MIC-1 in PC-3 cells, and apoptosis was also induced in this cell line but not in saPC-3 cell line suggesting a block in MIC-1 inducible apoptosis pathway.
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Powell, Nicole Damico. "Immunomodulation of experimental autoimmune encephalomyelitis targeting the autoreactive T cell and the cytokine macrophage migration inhibitory factor /". Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141052089.

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4

Nguyen, Tuyet Mai. "Elucidation of thiol-protein oxidoreductase activity of the cytokine macrophage migration inhibitory factor (MIF) by biochemical redox and site-specific mutagenesis analysis". [S.l. : s.n.], 2003. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10520514.

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5

Baeza, Garcia Alvaro. "Rôle de MIF (Macrophage Migration Inhibitory Factor) dans l'immunité innée et la réponse anti-schistosome chez Biomphalaria glabrata". Phd thesis, Université du Droit et de la Santé - Lille II, 2010. http://tel.archives-ouvertes.fr/tel-00665113.

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Schistosoma mansoni est un parasite helminthe responsable de la schistosomiase intestinale, qui affecte 200 millions de personnes dans les zones tropicales et subtropicales, et l'on estime que 600 millions de personnes sont exposées au risque de cette infection. Le cycle de vie du parasite est complexe et il requière, un hôte définitif, l'homme et un hôte intermédiaire, un mollusque d'eau douce appelé Biomphalaria glabrata. C'est chez le mollusque où le parasite se multiplie de forme massive de là l'importance du mollusque dans la transmission du parasite à l'homme. Lors de l'infection le mollusque met en place une réponse cellulaire et humorale très marquées pouvant dans certains cas tuer le parasite. Malgré l'importance du mollusque, les mécanismes moléculaires qui gouvernent ces réponses sont largement inconnus et donc l'étude de l'immunité du mollusque est une priorité en recherche médicale. Nous avons identifié deux orthologues de la cytokine de mammifère MIF (Macrophage Migration Inhibitory Factor ) BgMIF1 et BgMIF2. En utilisant des approches biochimiques et moléculaires en combinaison avec la technique de RNAi in vitro et in vivo nous avons démontré le rôle de BgMIF 1 et BgMIF2 comme régulateurs centrales de l'immunité innée du mollusque. En particulaire BgMIF1 régule l'activation des hémocytes et la réponse d'encapsulation lors de l'infection. D'un autre côté BgMIF2 régule dans la réponse antibactérienne. Nos résultats montrent que chez B. glabrata il y une régulation fine de la réponse immune innée et une capacité pour répondre de façon différente lors d'un challenge immunitaire. De plus une régulation par une cytokine de type vertébré dans un invertébré n'avait jusqu'à présent jamais été décrite. Nos travaux établissent les bases pour mieux comprendre les relations hôte-parasite dans une maladie comme la schistosomiase, et aussi constituent une avancée importante du point de vue de l'évolution de l'immunité innée en général.l
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Baía, Diogo Nogueira de Graça 1984. "Role of the LILRB1 HLA class I-specific inhibitory receptor in the regulation of macrophage function". Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/380898.

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Abstract (sommario):
In the present work the regulatory role played by the HLA class I (HLA-I)-specific LILRB1 inhibitory receptor in human macrophages (MΦ) was addressed. In vitro differentiated monocyte-derived M1 and M2 MΦ expressed different LILRB1 levels. We provide experimental evidence supporting that LILRB1-HLA-I interaction regulated the MΦ activation threshold, controlling cytokine secretion under steady state as well as in response to tumor cells and to signaling through activating receptors. On the other hand, our observations support that LILRB1 binding to cells occurred independently of total HLA-I expression levels, correlating with HLA-I dimerization. Such conformational change was detectable in type I IFN-treated MΦ and associated to an enhanced LILRB1-HLA-I interaction, thus providing a potential regulatory mechanism to control MΦ activation
En aquest projecte hem analitzat la participació del receptor inhibidor específic per HLA de classe I: LILRB1, en la regulació de la funció dels macròfags humans (MΦ). Els macròfags M1 i M2 diferenciats in vitro expressen nivells diferents de LILRB1. Aportem evidències experimentals que recolzen el paper de la interacció LILRB1/HLA-I com element regulador del llindar d’activació en la homeòstasi del macròfag, influint en la secreció de citocines en condicions basals així com en resposta a cèl.lules tumorals i a la senyalització de receptors activadors dependents de motius ITAM. D’altra banda, les nostres observacions indiquen que el reconeixement de cèl.lules diana per part de LILRB1 es dóna independentment del nivell d’expressió de les molècules del HLA en la seva superfície, però correlaciona amb la dimerització d’aquestes molècules. Aquest canvi conformacional, detectat en MΦ tractats amb interferons de tipus I, s’associa a un increment de la interacció entre LILRB1 i HLA-I, suggerint un possible mecanisme regulador de l’activació del MΦ.
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Rasiah, Krishan Kumar St Vincent's UNSW. "The identification of novel biomarkers in the development and progression of early prostate cancer". Awarded by:University of New South Wales. St Vincent's, 2006. http://handle.unsw.edu.au/1959.4/24187.

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ABSTRACT The morphological premalignant changes in prostate epithelium such as high grade prostatic intraepithelial neoplasia (HGPIN) precede invasive prostate cancer (PC) by several decades. The overall aim of this project was to identify patterns of gene expression in HGPIN and early PC which increase our understanding of the early biology of PC and identify genes and pathways that correlate with an aggressive phenotype. A comprehensive tissue cohort of premalignant prostate lesions was collected in a tissue microarray (TMA) platform that was utilised for high-throughput validation of target genes. Using this unique resource, the expression of the tumour suppressor gene PTEN was assessed using immunohistochemistry in an initial candidate gene approach based on mouse models implicating PTEN in carcinogenesis. No significant difference in expression of PTEN was detected in premalignant and benign epithelium. A transcript profiling approach was undertaken by integrating laser capture microdissection, linear RNA amplification and oligonucleotide microarrays to perform a screen of matched patient samples of normal, HGPIN and PC cells. The expression patterns of two genes encoding secreted proteins, neuropeptide Y (NPY) and macrophage inhibitory cytokine (MIC-1) were validated using immunohistochemistry on TMAs representing the progression model of early PC. Increased expression of these proteins in PC was confirmed to occur early in the disease process and altered expression of NPY and MIC-1 was associated with worse clinical outcome. Further analysis of global gene expression patterns using a structured network knowledge base identified a notable aberration in the expression of extracellular matrix and extracellular matrix associated proteins in HGPIN and provided novel evidence for the role of this class of molecules in the development of PC. In summary, contrary to current dogma based on work in animal models, altered PTEN expression is unlikely to represent an important event in the development of malignancy in the human prostate. In contrast, the expression patterns and prognostic value of NPY and MIC-1 in HGPIN support their further evaluation as biomarkers for the development and progression of PC. The aberrant expression of genes and networks of genes detected in HGPIN will assist in further identification of biological pathways which may be targeted in therapeutic strategies against the development and progression of PC.
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Lacey, Derek. "NFκB independent pathway activation of rheumatoid arthritis FLS by macrophage migration inhibitory factor (MIF)". Monash University, Faculty of Medicine, 2003. http://arrow.monash.edu.au/hdl/1959.1/9457.

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9

Lo, Wing-sze, e 盧詠詩. "The role of macrophage migration inhibitory factor in the pathogenesisof acute graft-versus-host disease following allogeneic bone marrowtransplantation". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31226413.

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Michelet, Claire. "Analyse évolutive et fonctionnelle des Macrophage Migration Inhibitory Factors chez les eucaryotes". Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4109/document.

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Les cytokines MIFs (Macrophage Migration Inhibitory Factor) sont des protéines multifonctionnelles qui, chez les mammifères, interviennent dans plusieurs processus majeurs tels que le contrôle du cycle et de la mobilité cellulaire, l’activation de la réponse immunitaire et l’inhibition de l’apoptose. Des travaux récents montrent que les protéines MIFs peuvent également jouer un rôle majeur dans l’immunité des invertébrés, et être utilisées par des organismes parasites d’animaux ou de végétaux pour inhiber les défenses de leurs hôtes respectifs, ce qui soulève la question de leur diversité, de leur histoire évolutive et des potentielles différences fonctionnelles. L’objectif général de ce travail de thèse était d’explorer la diversité et l’histoire évolutive des protéines MIFs à une échelle trans-règne, puis de rechercher leurs éventuelles différences fonctionnelles, en se focalisant sur les systèmes plantes-pathogènes. Nous avons tout d’abord identifié les MIFs chez 803 espèces de plantes, champignons, protistes, et métazoaires, et analysé leur présence/absence et histoire évolutive en fonction des taxa, de l’écologie et du mode de vie (libre ou parasitaire) des espèces. Nous avons montré que l’histoire évolutive des MIFs, chez les eucaryotes, est complexe et implique des duplications ancestrales ainsi que des pertes multiples ou des re-duplications récentes. Les plantes (espèces libres autotrophes) et les parasites de plantes (autres que champignons) possèdent un nombre médian de trois MIFs, alors que les espèces hétérotrophes et les parasites d’animaux ont un nombre de MIF plus faible et/ou plus variable. De plus, les protéines MIFs semblent essentielles et fortement conservées, avec de nombreux résidus sous sélection purifiante, chez certains groupes comme les plantes, alors que dans d’autres groupes, elles semblent facultatives (e.g. champignons) ou présentes en plusieurs copies divergentes (e.g. nématodes, insectes), ce qui suggère de potentielles néofonctionalisations. Nous avons ensuite analysé l’effet des protéines MIFs de plusieurs espèces sur la mort cellulaire en système végétal. Tous les organismes testés (plantes oomycètes, protozoaires, insectes et nématodes), y compris ceux n’ayant pas d’interaction avec les plantes, possèdent au moins une protéine MIF capable d’inhiber cette mort cellulaire. Cela suggère que l’inhibition de la mort cellulaire en plante ne correspond pas à une néofonctionalisation des MIFs de parasites de plantes, mais serait liée à des propriétés structurales et conservées des MIFs. Toutefois, aucun des paramètres étudiés (localisation subcellulaire) ou prédits in silico (présence de motifs, structures 3D, oligomérisation, modifications post-traductionnelles) ne semble lié à cette activité d’inhibition de la mort cellulaire. De futures études fonctionnelles poussées sont nécessaires à l’élucidation des relations structure/fonction de ces protéines complexes
Macrophage migration inhibitory factors (MIF) are multifunctional proteins regulating major processes in mammals, including control of the cell cycle and migration, activation of innate immune responses, and prevention of p53-mediated apoptosis. MIF proteins also play a role in innate immunity of invertebrate organisms or serve as virulence factors in parasitic organisms, raising the question of their evolutionary history and of a putative differential evolution of structure/function relationships. The general aim of this PhD was to explore the diversity and evolutionary history of MIF proteins accross kingdoms, and to investigate their potential functional differences, with a special emphasis on host-parasite systems. We first performed a broad survey of MIF presence or absence and evolutionary relationships across 803 species of plants, fungi, protists, and animals, and explored a potential relation with the taxonomic status, the ecology, and the lifestyle of individual species. We show that MIF evolutionary history in eukaryotes is complex, involving ancestral duplications, multiple gene losses and recent clade-specific re-duplications. Of note, plants and plant parasites (other than fungi) harbour a median number of three MIFs, while heterotrophic and animal parasite species harbour a lower or/and variable MIF number. Intriguingly, MIFs seem to be essential and highly conserved with many sites under purifying selection in some kingdoms (e.g. plants), while in other kingdoms they appear more dispensable (e.g. in fungi) or present in several diverged variants (e.g. insects, nematodes), suggesting potential neofunctionalizations within the protein superfamily. We then analysed the effect of MIF proteins from selected species on plant cell death. All organisms tested (plant, oomycetes, protozoa, insects, and nematodes) including species that are not in interaction with plants, possess at least one MIF protein showing a significant cell death inhibitory effect. This suggests that plant cell death inhibition does not result from a neofunctionalization of MIF from plant-parasites, and is related to conserved structural features of MIF proteins. However, none of the parameters predicted in silico (sequence motifs, 3D structures, oligomerization, post-traductional modifications) appeared to be related to the cell death inhibitory activity. Future extensive functional studies are necessary to unravel the structure-function relationship of these evolutionarily and functionally complex proteins
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Libri sul tema "Macrophage inhibitory cytokine"

1

Bucala, Richard. Mif Handbook. World Scientific Publishing Co Pte Ltd, 2012.

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2

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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Berry, Martin, e Ann Logan. CNS Injuries: Cellular Responses and Pharmacological Strategies (Pharmacology & Toxicology (Crc Pr)). CRC, 1998.

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M, Berry, e Logan Ann, a cura di. CNS injuries: Cellular responses and pharmacological strategies. Boca Raton: CRC Press, 1999.

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Capitoli di libri sul tema "Macrophage inhibitory cytokine"

1

Feng, Lili, Byeong C. Jang e Daniel Hwang. "Inhibitor of Protein Tyrosine Kinase, Radicicol, Suprresses the Expression of Cyclooxygenase and Pro-Inflammatory Cytokines in LPS-Stimulated Rat Alveolar Macrophage in Part by Accelerating Degradation of mRNA". In Advances in Experimental Medicine and Biology, 281–88. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1813-0_42.

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"Macrophage Inhibitory Cytokine 1". In Encyclopedia of Cancer, 2609. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_101405.

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ARENBERG, D., e R. BUCALA. "Macrophage migration inhibitory factor (MIF)". In The Cytokine Handbook, 1037–48. Elsevier, 2003. http://dx.doi.org/10.1016/b978-012689663-3/50049-1.

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"Macrophage Migration Inhibitory Factor (MIF )". In Cytokine Gene Polymorphisms in Multifactorial Conditions, 219–34. CRC Press, 2006. http://dx.doi.org/10.1201/9781420005325-22.

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Alourfi, Zaynab, David Ray e Rachelle Donn. "Macrophage Migration Inhibitory Factor (MIF)". In Cytokine Gene Polymorphisms in Multifactorial Conditions, 191–205. CRC Press, 2006. http://dx.doi.org/10.1201/9781420005325.ch14.

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Fleischmann, Roy. "Signalling pathway inhibitors". In Oxford Textbook of Rheumatology, 630–35. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081_update_003.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and other pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Many of the pro-inflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Spleen tyrosine kinase (SyK) is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling should interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib, approved in many countries for the treatment of RA, is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2; there are other JAK inhibitors in development which are purported to be more specific for JAK3 (Vertex 509), specific for JAK1/2 (baricitinib) or more specific for JAK1 (Galapagos and INCYTE) where clinical data has been reported. Tofacitinib has been investigated in multiple clinical trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎‎) and in patients who have failed TNFα‎‎ inhibitors. Vertex 509 has been investigated as monotherapy or in combination with MTX in DMARD failures while baricitinib, GLPG0634 (Galapagos), and INCB039110 (Incyte) have been investigated in phase 1 and 2 clinical trials in combination with MTX. Each of these medications has demonstrated efficacy; their safety profile has been shown to be generally similar although with some differences from each other and some differences from most of the currently approved biological agents. Fostamatinib disodium is an orally available inhibitor of SyK which was investigated in multiple phase 3 clinical trials in RA but was found to be generally ineffective with significant safety signals. This chapter discusses what is currently known and understood about the efficacy and safety of these oral, small-molecule DMARDs.
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Cheng, Jianguo. "Mechanisms of Neuropathic Pain". In Neuropathic Pain, a cura di Jianguo Cheng, 17–26. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190298357.003.0003.

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Neuropathic pain arises as a direct consequence of a lesion or a disease affecting the somatosensory system. The mechanisms of neuropathic pain are often complex and difficult to study given the diversity of causes, pathology, and clinical presentation of various neuropathic pain conditions. Common mechanisms include peripheral and central sensitizations. Peripheral sensitization refers to increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields. Central sensitization refers to the augmented response of central signaling neurons. The mechanisms of peripheral and central sensitization are understood at the cellular and molecular levels. The processes of neuroplasticity involve activation of inflammatory cells, such as macrophages (and microglia in the central nervous system) and other immune cells, and release of inflammatory mediators, such as cytokines, chemokines, and a host of other mediators. Interactions of these mediators with specific receptors in the nociceptors or the spinal cord neurons may lead to phosphorylation or changes in expression of ion channels, receptors, transporters, and other effectors through specific signaling pathways. These events ultimately lead to changes in excitability, conductivity, and transmissibility of neurons in the pain processing pathways. Other factors may include disinhibition of interneurons, changes in descending inhibitory and excitatory pathways, and reorganization of the cortical areas and their interconnections.
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"Eicosanoid Inhibitor and Cytokine Regulation of 1,25(OH)2D3 Synthesis in Synovial Fluid Macrophages from Patients with Inflammatory Arthritis". In Vitamin D, 145–46. De Gruyter, 1994. http://dx.doi.org/10.1515/9783110882513-051.

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Atti di convegni sul tema "Macrophage inhibitory cytokine"

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Karan, Dev, Seema Dubey, Jo Wick, Ossama Tawfik, Guru Sonpavde e Peter VanVeldhuizen. "Abstract B12: Macrophage inhibitory cytokine-1 as a potential biomarker for racial disparity in prostate cancer". In Abstracts: Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; November 13-16, 2015; Atlanta, Georgia. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7755.disp15-b12.

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Jin, Young-June, Jeong-Hyung Lee, Young-Myeong Kim, Keun-Cheol Kim e Hansoo Lee. "Abstract 3041: Macrophage inhibitory cytokine-1 stimulates proliferation of human umbilical vein endothelial cells by up-regulating Cyclins D1 and E through the PI3K/Akt- and ERK-dependent AP-1 and E2F activation signaling pathways". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3041.

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Segal, Leopoldo, Rohan Kulkarni, Yoko Fujita, Anna Nolan, William N. Rom e Michael Weiden. "Azithromycin Suppresses Inflammatory Cytokines And Induces Inhibitory Transcription Factors In Alveolar Macrophages". In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2853.

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Lin, E., F. Vincent, J. Harris, R. Kandane-Rathnayake, G. S. Ngian, J. Sahhar, E. Morand e T. Lang. "THU0403 Serum levels of macrophage migration inhibitory factor and interleukin-1 family cytokines are elevated in systemic sclerosis". In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3272.

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Charron, Catherine, Matthew Coates, Kazuhiro Ito, Chaitanya Vuppusetty, Masako To, John Murray, Peter Strong e Garth Rapeport. "Superior Effects Of RV1088, A Novel Narrow Spectrum Kinase Inhibitor, To BIRB796, A P38MAPK Inhibitor, On Pro-Inflammatory Cytokine Production In Macrophages". In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4538.

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Charron, Catherine, Matthew Coates, Kazuhiro Ito, Chaitanya Vuppusetty, Masako To, John Murray, Peter Strong e Garth Rapeport. "Superior Effects Of RV568, A Novel Narrow Spectrum Kinase Inhibitor, To BIRB796, A P38MAPK Inhibitor, On Pro-Inflammatory Cytokine Roduction In Macrophages". In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3088.

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Choudhary, Shilpa, James R. Pruitt, Thais M. Sielecki, Carol Pilbeam e John Arthur Taylor. "Abstract 159: Macrophage Migration Inhibitory Factor (MIF) enhances proliferation and expression of tumorigenic cytokines in a bladder cancer cell line". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-159.

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Kaur, Manminder, Matthew Beardsall, Michael Salmon e Dave Singh. "GS-5759, A Novel Bi-Functional Phosphodiesterase 4 Inhibitor And Long-Acting ²2-Adrenoceptor Agonist Inhibits Cytokine Production From COPD Alveolar Macrophages". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5705.

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Speth, J., L. R. K. Penke, J. D. Bazzill, J. J. Moon e M. Peters-Golden. "Synthetic Liposome Mimics of Alveolar Macrophage-Derived Vesicles Containing Suppressor of Cytokine Signaling 3: Inhibitors of Lung Tumor Cell Expansion and Potential Therapeutic for Lung Cancer". In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7433.

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Dres, Martin, Alexis Ferre, Amparo Buenestado, Stanislas Grassin Delyle, Emmanuel Naline, Nicolas Roche e Philippe Devillier. "Comparison Of A Cytokine Pattern Produced By Human Lung Macrophages And Pulmonary Parenchyma Explants In Response To Lipopolysaccharide And To A Cigarette Smoke Extract. Inhibitory Effect Of Budesonide". In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2856.

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