Bibliografie tematiche / Macrophage inhibitory cytokine - 1

Letteratura scientifica selezionata sul tema "Macrophage inhibitory cytokine - 1"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 10 febbraio 2022

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Articoli di riviste sul tema "Macrophage inhibitory cytokine - 1"

1

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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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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Abstract (sommario):
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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Singla, Reetu D., Jing Wang e Dinender K. Singla. "Regulation of Notch 1 signaling in THP-1 cells enhances M2 macrophage differentiation". American Journal of Physiology-Heart and Circulatory Physiology 307, n. 11 (1 dicembre 2014): H1634—H1642. http://dx.doi.org/10.1152/ajpheart.00896.2013.

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Macrophage polarization is emerging as an important area of research for the development of novel therapeutics to treat inflammatory diseases. Within the current study, the role of Notch1R in macrophage differentiation was investigated as well as downstream effects in THP-1 monocytes cultured in “inflammation mimicry” media. Interference of Notch signaling was achieved using either the pharmaceutical inhibitor DAPT or Notch1R small interfering RNA (siRNA), and Notch1R expression, macrophage phenotypes, and anti- and proinflammatory cytokine expression were evaluated. Data presented show that Notch1R expression on M1 macrophages as well as M1 macrophage differentiation is significantly elevated during cellular stress ( P < 0.05). However, under identical culture conditions, interference to Notch signaling via Notch1R inhibition mitigated these results as well as promoted M2 macrophage differentiation. Moreover, when subjected to cellular stress, macrophage secretion of proinflammatory cytokines was significantly heightened ( P < 0.05). Importantly, Notch1R inhibition not only diminished proinflammatory cytokine secretion but also enhanced anti-inflammatory protein release ( P < 0.05). Our data suggest that Notch1R plays a pivotal role in M1 macrophage differentiation and heightened inflammatory responses. Therefore, we conclude that inhibition of Notch1R and subsequent downstream signaling enhances monocyte to M2 polarized macrophage outcomes and promotes anti-inflammatory mediation during cellular stress.
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Huang, Mingguo, Shintaro Narita, Takamitsu Inoue, Norihiko Tsuchiya, Shigeru Satoh, Hiroshi Nanjo, Takehiko Sasaki e Tomonori Habuchi. "Diet-induced macrophage inhibitory cytokine 1 promotes prostate cancer progression". Endocrine-Related Cancer 21, n. 1 (febbraio 2014): 39–50. http://dx.doi.org/10.1530/erc-13-0227.

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Recent studies have indicated that a high-fat diet (HFD) plays an important role in prostate cancer (PCa) progression. Palmitic acid (PA) is one of the most abundant saturated free fatty acids (FAs) and is associated with carcinogenesis. In this study, we investigated the mechanism underlying the association of dietary fat, including PA, with PCa progression. In four PCa cell lines,in vitroPA administration stimulated the expression of macrophage inhibitory cytokine 1 (MIC1), which is a divergent member of the transforming growth factor-β family.In vivo, LNCaP xenograft tumor growth, serum MIC1 levels, and FA levels in xenograft tumors were significantly higher in mice receiving an HFD containing high amounts of PA than in those receiving a low-fat diet (LFD). In addition, tumor cells with high MIC1 expression invaded to venules and lymph vessels in the LNCaP xenograft.In vitrostudies showed that proliferation and invasive capacity were significantly higher in PCa cells cultured with serum from HFD-fed mice than in those cultured with the serum from LFD-fed mice. This effect was attenuated by the addition of neutralizing antibodies against MIC1, but not by isotype control antibodies. Clinically, serum MIC1 levels were significantly higher in PCa patients than in healthy controls, and higher levels were associated with higher pathological grade and obesity. In conclusion, our results indicate that an HFD containing PA may promote growth and invasiveness of PCa cells through the upregulation of MIC1 expression.
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Yamashita, Toshiharu, Akihiro Yoneta e Tokimasa Hida. "Macrophage Inhibitory Cytokine-1: A New Player in Melanoma Development". Journal of Investigative Dermatology 129, n. 2 (febbraio 2009): 262–64. http://dx.doi.org/10.1038/jid.2008.366.

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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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Andreone, Teresa, Gordon P. Meares, Katherine J. Hughes, Polly A. Hansen e John A. Corbett. "Cytokine-mediated β-cell damage in PARP-1-deficient islets". American Journal of Physiology-Endocrinology and Metabolism 303, n. 2 (15 luglio 2012): E172—E179. http://dx.doi.org/10.1152/ajpendo.00055.2012.

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Poly(ADP)-ribose polymerase (PARP) is an abundant nuclear protein that is activated by DNA damage; once active, it modifies nuclear proteins through attachment of poly(ADP)-ribose units derived from β-nicotinamide adenine dinucleotide (NAD+). In mice, the deletion of PARP-1 attenuates tissue injury in a number of animal models of human disease, including streptozotocin-induced diabetes. Also, inflammatory cell signaling and inflammatory gene expression are attenuated in macrophages isolated from endotoxin-treated PARP-1-deficient mice. In this study, the effects of PARP-1 deletion on cytokine-mediated β-cell damage and macrophage activation were evaluated. There are no defects in inflammatory mediator signaling or inflammatory gene expression in macrophages and islets isolated from PARP-1-deficient mice. While PARP-1 deficiency protects islets against cytokine-induced islet cell death as measured by biochemical assays of membrane polarization, the genetic absence of PARP-1 does not effect cytokine-induced inhibition of insulin secretion or cytokine-induced DNA damage in islets. While PARP-1 deficiency appears to provide protection from cell death, it fails to provide protection against the inhibitory actions of cytokines on insulin secretion or the damaging actions on islet DNA integrity.
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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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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 &gt; 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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Hayes, V. M. "Macrophage Inhibitory Cytokine-1 H6D Polymorphism, Prostate Cancer Risk, and Survival". Cancer Epidemiology Biomarkers & Prevention 15, n. 6 (1 giugno 2006): 1223–25. http://dx.doi.org/10.1158/1055-9965.epi-06-0063.

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Brown, D. A., F. Lindmark, P. Stattin, K. Balter, H. O. Adami, S. L. Zheng, J. Xu et al. "Macrophage Inhibitory Cytokine 1: A New Prognostic Marker in Prostate Cancer". Clinical Cancer Research 15, n. 21 (20 ottobre 2009): 6658–64. http://dx.doi.org/10.1158/1078-0432.ccr-08-3126.

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Tesi sul tema "Macrophage inhibitory cytokine - 1"

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 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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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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Montero, Rosa Maria. "Chemokines and macrophage migration inhibitory factor in diabetic nephropathy". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29851.

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Introduction: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease in the Western world. Aim: To determine whether macrophage migration inhibitory factor (MIF), monocyte chemoattractant protein-1 (MCP-1) or CC chemokine ligand 18 (CCL18) have a causative role in the development of renal inflammation and fibrosis in DN and are useful biomarkers of disease progression. Methods: Urine and plasma samples were collected from 115 DM and 116 Non-DM at baseline, previously analysed for MCP-1 and CCL18 ELISA by Dr Qureshi. I measured MIF in these samples and collected 107 DM and 114 Non-DM data points (GFR, ACR/UPCR and clinical parameters) at >18 months and >3 years. MIF, MCP-1 and CCL18 urine, plasma and serum analysis was performed in 42 DM and 60 Non-DM at >3 years follow up. Intrinsic renal cells were cultured and stimulated with diabetic conditions. These cytokines and fibronectin were measured in tubuloepithelial cells and podocytes. Results: Baseline plasma CCL18 and MIF predicted a decline in GFR in DM at >18 months but not at >3 years. Cytokine production varies over time with significant correlations at baseline that are not maintained. Cytokines correlate differently with GFR, ACR/UPCR in DM versus Non-DM proteinuric renal diseases. Plasma and serum cytokine levels correlated significantly with no correlation between these and urinary levels. All intrinsic renal cells were able to produce MIF, MCP-1 and CCL18 following stimulation. The interaction of these cytokines and their effects on fibronectin vary in diabetic conditions and following recombinant cytokine stimulation. The diabetic environment appears to orchestrate cytokine signals according to cell type. Conclusion: These results suggest cytokines may play a key role in the pathogenesis and or progression of DN. The clinical study suggests cytokines may predict progression; however, larger studies are needed with samples taken at different time points.
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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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Russell, Kirsty. "The role of macrophage migration inhibitory factor in airways disease". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/23917.

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Chronic obstructive pulmonary disease (COPD) and severe asthma are progressive chronic inflammatory diseases of the airways. Both diseases are characterised by airflow limitation and share some pulmonary symptoms. However they have distinct inflammatory cell signatures and differ in response to corticosteroid (CS) treatment. Most asthmatic patients control their disease with CS, with a few showing a relative CS resistance; however COPD patients show little or no improvement with CS and are CS insensitive. Macrophage migration inhibitory factor (MIF) is a pleiotropic pro-inflammatory mediator whose function is yet to be fully elucidated. MIF has been shown to counter-act the immunosuppressive action of CS. MIF is elevated in chronic diseases such as asthma and atherosclerosis. The role of MIF in COPD has not been investigated and its role in asthma is not fully understood. MIF inhibition attenuated ozone-induced airway inflammation and lung function in vivo but did not affect CS sensitivity. MIF expression did not vary between stable COPD patients and controls. Pro-inflammatory effects of MIF were investigated in THP-1 monocytes and primary cells. There was no clear role for MIF in LPS-induced inflammation. MIF modulated the transactivation functions of CS in THP-1 cells. Finally I took an unbiased approach to generate new hypotheses for MIF function using proteomic and transcriptomic techniques. The RIG-I-like pathway was identified by proteomics as a novel target pathway and was investigated in THP-1 cells and human BAL macrophage samples following viral infection. The role of MIF in airway inflammation remains unclear and results demonstrated here show MIF function does not necessarily translate from mouse to humans. MIF does not seem to have a role in the inflammation of stable disease. The proteomic data suggests that the association between viral infection, MIF and CS in regulating CS sensitivity in COPD and severe asthma should be investigated.
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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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Liu, Yu. "The role of suppressors of cytokine signalling 1 and 3 in macrophage activation". Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24848.

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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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Abstract (sommario):
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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Tamaki, Hiroyuki. "Human thioredoxin-1 ameliorates experimental murine colitis in association with suppressed macrophage inhibitory factor production". Kyoto University, 2007. http://hdl.handle.net/2433/135755.

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Libri sul tema "Macrophage inhibitory cytokine - 1"

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Harris, James, e Eric F. Morand, a cura di. Macrophage Migration Inhibitory Factor. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-4939-9936-1.

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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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Pitzalis, Costantino, Frances Humby e Michael P. Seed. Synovial pathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0052.

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Synovial pathology is seen in a variety of disease states, including rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis, and systemic lupus erythmatosus (SLE). This chapter highlights recent advances that characterize the cellular composition of these tissues according to surface markers and chemokine and cytokine expression, and describes synovial functional status and response to therapeutics. In RA, after initiation, pannus migrates over and under cartilage, and into subchondral bone, in a destructive process. Cartilage-pannus junction (CPJ) is characterized as invasive or 'quiescent' or 'indistinct'. Invasive CPJ can comprise macrophages, fibroblast-like synoviocytes (FLS), mast cells, and/or neutrophils. CPJ activity is related to the state of activation of the overlying subintima. Subintimal inflammation can be graded to a variety of degrees (I–IV) according to established criteria and is illustrated. In some RA synovia, cellular aggregates organize into ectopic lymphoid structures (ELS) through the expression of lymphorganogenic signals, to exhibit T- or B-cell zones accompanied by dendritic cells and lymphangiogenesis. ELS synthesize rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACAP), considered to be indicative of aggressive disease. The selective cellular expression of macrophage and dendritic cell chemokines and cytokines such as TNF, GMCSF, TGFβ‎, IL-1, IL-6, IL-23, and chemokines can be seen in synovia, to form a regulated and cooperative environment that sustains the cellular organization and pathological function. Important to this process are FLS and CD68+ macrophages. CD68 expression correlates with disease severity and can be useful as a surrogate marker of disease modifying activity of therapeutics, such as anti-TNF and anti-B-cell biologics.
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Capitoli di libri sul tema "Macrophage inhibitory cytokine - 1"

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Holdenrieder, S. "Macrophage migration inhibitory factor". In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_2007-1.

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Hoffmann, Adrian, Leon Christian Zwißler, Omar El Bounkari e Jürgen Bernhagen. "Studying the Pro-Migratory Effects of MIF". In Macrophage Migration Inhibitory Factor, 1–18. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_1.

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Abidi, Jawad H., James Harris e Nadia S. Deen. "Co-Immunoprecipitation of Macrophage Migration Inhibitory Factor". In Macrophage Migration Inhibitory Factor, 115–22. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_10.

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Graham, Amanda, e Warren B. Nothnick. "Concurrent Immunohistochemical Localization and Western Blot Analysis of the MIF Receptor, CD74, in Formalin-Fixed, Paraffin-Embedded Tissue". In Macrophage Migration Inhibitory Factor, 123–34. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_11.

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Gu, Ran. "Methods to Determine the Effects of MIF on In Vitro Osteoclastogenesis Using Murine Bone Marrow-Derived Cells and Human Peripheral Blood Mononuclear Cells". In Macrophage Migration Inhibitory Factor, 135–45. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_12.

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Deen, Nadia S., Jacinta P. Lee e James Harris. "Inducing and Inhibiting Autophagy to Investigate Its Interactions with MIF". In Macrophage Migration Inhibitory Factor, 147–58. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_13.

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Pinar, Anita A., e James Harris. "Assays for Measuring the Role of MIF in NLRP3 Inflammasome Activation". In Macrophage Migration Inhibitory Factor, 159–72. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_14.

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Zamani, Shahrzad, Eric F. Morand e Jacqueline K. Flynn. "Assays for Inducing and Measuring Cell Death to Detect Macrophage Migration Inhibitory Factor (MIF) Release". In Macrophage Migration Inhibitory Factor, 173–83. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_15.

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Aitken, Elizabeth H. "Assessing the Role of MIF in Plasmodium spp. Infections Using Ex Vivo Models". In Macrophage Migration Inhibitory Factor, 185–92. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_16.

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Vujičić, Milica, Sanja Despotović, Tamara Saksida e Ivana Stojanović. "The Effect of Macrophage Migration Inhibitory Factor on Intestinal Permeability: FITC-Dextran Serum Measurement and Transmission Electron Microscopy". In Macrophage Migration Inhibitory Factor, 193–201. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9936-1_17.

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Atti di convegni sul tema "Macrophage inhibitory cytokine - 1"

1

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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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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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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Leung, CT. "PO-319 Role of stanniocalcin-1 on macrophage differentiation and cytokine production". In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.832.

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Veal, Antia E., Brandon Lam, Teresa Collins e Joseph Larkin. "AI-11 The kinase inhibitory region of suppressor of cytokine signaling-1 modulates autoinflammatory skin pathology". In LUPUS 21ST CENTURY 2018 CONFERENCE, Abstracts of the Fourth Biannual Scientific Meeting of the North and South American and Caribbean Lupus Community, Armonk, New York, USA, September 13 – 15, 2018. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-lsm.11.

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Lang, T., J. Lee, A. Pinar, H. Fan, A. Mansell, E. Morand e J. Harris. "344 Linking macrophage migration inhibitory factor and nlrp3 in the pathogenesis of il-1 dependent inflammatory disorders". In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.344.

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Chen, C. T., S. Park, M. Bhargava e P. A. Torzilli. "Inhibitory Effect of Mechanical Load on IL-1 Induced Cartilage Degradation Is Mediated by Interferon-Gamma and IL-1 Receptor 1". In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193230.

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Abstract (sommario):
Matrix remodeling in articular cartilage is regulated by the elevation and activation of aggrecanases (ADAMTS-4 and ADAMTS-5) and matrix metalloproteinases (MMPs) [2–4, 7–9, 10]. Several recent studies from our and other groups have shown that mechanical loading can counteract interleukin 1 (IL-1) induced pro-inflammatory and catabolic events by down-regulating aggrecanases, MMPs, and pro-inflammatory genes [1, 3, 5, 6], but the molecular mechanism is not clear. Many previous studies have shown that the regulation of pro-inflammatory effect of IL-1 come from several aspects: anti-inflammatory cytokines (TGF-β, IL-10, IL-6 and interferon γ), IL-1 receptor related proteins (IL-1R1, IL-1R2, and IL-1Ra) as well as a family of intracellular inhibitory protein called Suppressor Of Cytokine Signaling (SOCS.) SOCS1 and SOCS3 are especially important, since they can inhibit both MAPK and NF-κB pathways induced by IL-1 [12]. The objective of this study was to determine whether mechanical load affected anti-inflammatory mediators along with anti-catabolic events.
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Balogh, Kristen, e Janet Cross. "Abstract B63: The Macrophage Migration Inhibitory Factor promotes breast cancer metastasis through interaction with the host immune response". 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-b63.

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Zhu, Guiquan, Yaling Tang, Ling Li e Xinhua Liang. "Abstract 1547: Tumor-derived macrophage Migration Inhibitory Factor and interleukin-6 cooperated in hypoxic accumulation of CD11b+Gr-1+ myeloid cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1547.

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Mahalingam, Devalingam, Manish R. Patel, Jasgit C. Sachdev, Lowell L. Hart, Niels Halama, Ramesh K. Ramanathan, John Sarantopoulos et al. "Abstract CT046: First-in-human phase 1 study assessing imalumab (BAX69), an anti-oxidized macrophage migration inhibitory factor (oxMIF) antibody in advanced solid tumors". In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-ct046.

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