Our results demonstrate that the heat shock response is a potent inhibitor of RANTES gene expression in vitro. Induction of the heat shock response inhibited TNF-α-mediated expression of RANTES mRNA and secretion of immunoreactive RANTES. These effects were not secondary to cytotoxicity, and are consistent with previous data demonstrating that the heat shock response inhibited proinflammatory responses of lung cells (23, 24, 25, 26, 27). We propose that the observed inhibition is not a generalized effect of the heat shock response. Rather, it appears that the heat shock response has a relatively specific inhibitory effect on lung proinflammatory responses. Evidence to support this assertion includes the observation that the heat shock response did not affect surfactant protein gene expression in cultured respiratory epithelium (24). Moreover, the heat shock response increased I-κBα gene expression in cultured respiratory epithelium, a protein that normally functions to inhibit NF-κB nuclear ...
Buy our Recombinant Human RANTES protein. Ab87758 is a full length protein produced in Escherichia coli and has been validated in SDS-PAGE. Abcam provides free…
Hepatitis C virus (HCV) infection is associated with high percentage of chronicity which implies the ability of the virus to evade or modulate host cell immune system. Modulation of chemokines, such as RANTES may be part of the virus induced pathogenicity. We examined the effect of core and structural proteins of HCV on RANTES expression in two liver derived cell lines, HepG2 and Chang Liver (CHL). HepG2 and Chang Liver (CHL) cell lines were established and selected for constitutive expression of HCV core and structural genes. Flow cytometry and quantitative RT-PCR analysis were performed to examine the effect of HCV core protein on RANTES expression. Luciferase analysis after RANTES-Luc-promoter transfection of established cell lines was assayed by luminometer measurements (RLU) of RANTES promoter activity. IRF-1 and IRF-7 expression was then examined by immunoblotting analysis. Results of flow cytometry and RT-PCR analysis indicated that RANTES is differentially regulated by HCV core protein in the
TY - JOUR. T1 - Role of nerve growth factor in rantes expression by keratinocytes. AU - Raychaudhuri, Siba P. AU - Farber, E. M.. AU - Raychaudhuri, S. K.. PY - 2000. Y1 - 2000. N2 - A role of neurogenic inflammation induced by the neuropeptides and nerve growth factor (NGF) has been attributed to the pathogenesis of several cutaneous disorders such as psoriasis, wound healing and eczematous dermatitis. The underlying mechanisms of the inflammatory process induced by NGF are not clearly established. This study explored whether NGF influences the inflammatory process by inducing chemokines. The effects of NGF were investigated on induction of 2 important chemokines, interleukin-8 and RANTES, which are known to be upregulated in the keratinocytes of various inflammatory conditions. NGF significantly increased RANTES production by the keratinocytes (p,0.001, 2-tailed Students t-test). Induction of RANTES expression in the keratinocytes by NGF provides further insight regarding the role of NGF-NGF ...
RANTES (regulated upon activation, normal T cell expressed and secreted) is released by cytotoxic T lymphocytes (CTL), and is a potent chemoattractant factor for monocytes and T cells, also known for its ability to suppress HIV infection. At micromolar concentration, RANTES is able to activate leukocytes, and, paradoxically, to enhance HIV infection in vitro. These latter properties are dependent on its ability to self-aggregate. In order to understand further the mechanism of RANTES-induced activation, the effects of both aggregated and disaggregated RANTES on antigen-specific CD8(+) clones were studied in comparison with the effects of specific antigens and in the presence of specific inhibitors of RANTES-mediated activation. We observed large amounts of RANTES aggregated on the cell surface, which led to cell activation, including up-regulation of cell surface markers, and secretion of IFN-gamma and macrophage inflammatory protein (MIP)-1beta. Specific inhibitors of RANTES-induced activation, such as
BioAssay record AID 52555 submitted by ChEMBL: Compound was tested in vitro for inhibition of [125I]RANTES binding to THP-1 cell membranes rich in C-C chemokine receptor type 1.
Granulomas form by a stepwise series of events, starting when T helper cells recognise protein peptides presented to them by antigen presenting cells bearing histocompatibility class II molecules. Immunological reactivity or inflammation attract monocyte macrophages which fuse to form multinucleated giant cells and onwards to epithelioid cells. Granuloma formation is aided by a cavalcade of chemotactic factors; Th1 cells induce interleukin (IL)-2, interferon gamma, and tumour necrosis factor (TNF) with the help of IL-12 and costimulator B7. The resulting exuberant granuloma formation is associated with active cell mediated hypersensitivity and tissue destruction. This framework is also remodelled by chemokines, adhesion molecules, matrix receptors of the integrin family, costimulators B7 and CD28, IL-12, and RANTES (regulated on activation normal T cells as secreted).. Bronchoalveolar fluid (BALF) reveals this macrophage class II-CD4Th1 cell synergy with its awesome cytokine cascade. Angiotensin ...
Blocking HIV-1 cell entry has long been a major goal of anti-HIV drug development. Here, we report a successful design of two highly potent chimeric HIV entry inhibitors composed of one CCR5-targeting RANTES (regulated on activation normal T cell expressed and secreted) variant (5P12-RANTES or 5P14-RANTES (Gaertner, H., Cerini, F., Escola, J. M., Kuenzi, G., Melotti, A., Offord, R., Rossitto-Borlat, I., Nedellec, R., Salkow-itz, J., Gorochov, G., Mosier, D., and Hartley, O. (2008) Proc. Natl. Acad. Sci. U.S.A. 105, 17706 -17711)) linked to a gp41 fusion inhibitor, C37. Chimeric inhibitors 5P12-linker-C37 and 5P14-linker-C37 showed extremely high antiviral potency in single cycle and replication-competent viral assays against R5-tropic viruses, with IC50 values as low as 0.004 nM. This inhi-bition was somewhat strain-dependent and was up to 100-fold better than the RANTES variant alone or in combination with unlinked C37. The chimeric inhibitors also fully retained the antiviral activity of C37 ...
ICAM-3 and CCR5 polarization induced by RANTES and (AOP)- RANTES in T lymphoblasts. (A) Time course of RANTES- and (AOP)- RANTES-induced ICAM-3 redistribution
AlphaLISA no-wash assay kit for detection and quantitation of Mouse/Rat C-C Motif Chemokine 5 / Regulated Upon Activation Normal T-Cell Expressed, and Secreted (CCL5/RANTES) in serum, bronchial lavage fluid (BALF), buffered solution or cell culture medium.
Rat monoclonal RANTES antibody [53405.111] validated for WB, ELISA, Inhibition and tested in Human and Mouse. With 1 independent review. Immunogen…
ELISA Kit for Regulated On Activation In Normal T-Cell Expressed And Secreted (RANTES), Hölzel Diagnostika, Produkte, ELISA, Human
canine CCL5/RANTES gene cDNA, cloning vector & expression plasmid, mutiple tags. Optimized for high expression in mammalian cells. Save up to 60%.
TY - JOUR. T1 - Regulation of RANTES promoter activation in gastric epithelial cells infected with Helicobacter pylori. AU - Kudo, Takahiko. AU - Lu, Hong. AU - Wu, Jeng Yih. AU - Graham, David Y.. AU - Casola, Antonella. AU - Yamaoka, Yoshio. PY - 2005/11. Y1 - 2005/11. N2 - RANTES, a CC chemokine, plays an important role in the inflammatory response associated with Helicobacter pylori infection. However, the mechanism by which H. pylori induces RANTES expression in the gastric mucosa is unknown. We cocultured gastric epithelial cells with wild-type H. pylori, isogenic oipA mutants, cag pathogenicity island. (PAI) mutants, or double knockout mutants. Reverse transcriptase PCR showed that RANTES mRNA was induced by H. pylori and that the expression was both OipA and cag PAI dependent. Luciferase reporter gene assays and electrophoretic mobility shift assays showed that maximal H. pylori-induced RANTES gene transcription required the presence of the interferon-stimulated responsive element ...
Chemokines are a family of cytokines involved in the extravasation of leukocytes to the site of inflammation. 4 CCL2/monocyte chemoattractant protein-1 (MCP-1), which is chemotactic for monocytes, 5 and CXCL8/IL-8, which chemoattracts neutrophils, 6 have been reported to be elevated in the bronchoalveolar lavage fluid (BALF) or serum of patients with active pulmonary sarcoidosis. 7 8 9 10 CCL3/macrophage inflammatory protein-1α (MIP-1α), CCL4/MIP-1β, and CCL5/regulated on activation normal T-cell expressed and secreted (RANTES) also have been shown to be elevated in the BALF of patients with pulmonary sarcoidosis. 11 12 13 As a result of the findings that CCL3 and CCL5 share the same CC chemokine receptor (CCR5) that is expressed abundantly on Th1-type cells and that CCR5 mRNA expression is upregulated in BALF of patients with pulmonary sarcoidosis, these chemokines have been suggested to be involved in the recruitment of Th1 cells 14 from the circulation to the granulomas in pulmonary ...
This study aimed to evaluate the effects of dioscorins isolated from 2 yam species, Dioscorea alata (Da-dioscorins) and Dioscorea japonica (Dj-dioscorins), on mouse immune activities. Results from cytokine array indicated that Dj-dioscorins increased the production of tumor necrosis factor (TNF)-α, interleukin (IL)-2, IL-3, IL-6, IL-10, IL-12p40, IL-13, monocyte chemoattractant protein (MCP)-1, regulated on activation, normal T cell expressed and secreted (RANTES), and granulocyte colony-stimulating factor (GCSF) in the spleen cells of BALB/c mice. In RAW264.7 macrophage, Da-dioscorins upregulated the expression of TNF-α, IL-1β, IL-6, IL-10, RANTES, MCP-1, and GCSF genes to a greater extent than Dj-dioscorins did. TNF-α, IL-1β, IL-6, IL-10, and RANTES gene expression was higher in spleen cells than in bone marrow and thymus cells in Da-dioscorin- or Dj-dioscorin-treated BALB/c and C57BL/6. Overall, our results suggest that dioscorins exert distinct immunomodulatory effects on mouse immune ...
Intestinal epithelial cells are the initial sites of host response to Clostridium difficile infection and can play a role in signaling the influx of inflammatory cells. To further explore this role, the regulated expression and polarized secretion of CXC and CC chemokines by human intestinal epithelial cells were investigated. An expression of the CXC chemokines, including IL-8 and growth-related oncogene (GRO)-alpha, and the CC chemokine monocyte chemoattractant protein (MCP)-1 from HT-29 cells increased in the 1-6 hr following C. difficile toxin A stimulation, assessed by quantitative RT-PCR. In contrast, the expression of neutrophil activating protein-78 (ENA-78) was delayed for 18 hr. The up-regulated mRNA expression of chemokines was paralleled by the increase of protein levels. However, the expression of macrophage inflammatory protein (MIP)-1alpha, RANTES (regulated on activation normal T cells expressed and secreted), and interferon-gamma-inducible protein-10 (IP-10) was not changed in ...
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Background Statins have previously been proven to lessen the in vitro disease of human being immunodeficiency pathogen type 1 (HIV-1) through modulation of Rho GTPase activity and lipid raft formation in the cell surface area as well while by disrupting LFA-1 incorporation into viral contaminants. of CCR5 mRNA manifestation. The CC-chemokine RANTES protein and mRNA expression levels were increased in CD4+ enriched lymphocytes treated with statins somewhat. Both X4 and R5 HIV-1 were reduced for his or her infection of statin-treated cells; however in ethnicities where statins had been removed and in which a reduction in CCR5 manifestation was observed there is a preferential inhibition of disease with an R5 versus X4 pathogen. Conclusions The outcomes indicate how the modulation of CC-chemokine receptor (CCR5) and CC-chemokine (RANTES) manifestation levels is highly recommended as adding to the anti-viral ramifications of statins preferentially inhibiting R5 infections. This observation in ...
Chemoattractant for blood monocytes, memory T-helper cells and eosinophils. Causes the release of histamine from basophils and activates eosinophils. May activate several chemokine receptors including CCR1, CCR3, CCR4 and CCR5. One of the major HIV-suppressive factors produced by CD8+ T-cells. Recombinant RANTES protein induces a dose-dependent inhibition of different strains of HIV-1, HIV-2, and simian immunodeficiency virus (SIV). The processed form RANTES(3-68) acts as a natural chemotaxis inhibitor and is a more potent inhibitor of HIV-1-infection. The second processed form RANTES(4-68) exhibits reduced chemotactic and HIV-suppressive activity compared with RANTES(1-68) and RANTES(3-68) and is generated by an unidentified enzyme associated with monocytes and neutrophils (PubMed:16791620, PubMed:1380064, PubMed:8525373, PubMed:9516414, PubMed:15923218). May also be an agonist of the G protein-coupled receptor GPR75, stimulating inositol trisphosphate production and calcium mobilization ...
Chemokine (C-C motif) ligand 5 (also CCL5) is a protein which in humans is encoded by the CCL5 gene. It is also known as RANTES (regulated on activation, normal T cell expressed and secreted). CCL5 is an 8kDa protein classified as a chemotactic cytokine or chemokine. CCL5 is chemotactic for T cells, eosinophils, and basophils, and plays an active role in recruiting leukocytes into inflammatory sites. With the help of particular cytokines (i.e., IL-2 and IFN-γ) that are released by T cells, CCL5 also induces the proliferation and activation of certain natural-killer (NK) cells to form CHAK (CC-Chemokine-activated killer) cells. It is also an HIV-suppressive factor released from CD8+ T cells[citation needed]. This chemokine has been localized to chromosome 17 in humans. RANTES was first identified in a search for genes expressed late (3-5 days) after T cell activation. It was subsequently determined to be a CC chemokine and expressed in more than 100 human diseases. RANTES expression is ...
CCL5 is an 8kDa protein classified as a chemotactic cytokine or chemokine. CCL5 is chemotactic for T cells, eosinophils, and basophils, and plays an active role in recruiting leukocytes into inflammatory sites. With the help of particular cytokines (i.e., IL-2 and IFN-γ) that are released by T cells, CCL5 also induces the proliferation and activation of certain natural-killer (NK) cells to form CHAK (CC-Chemokine-activated killer) cells.[6] It is also an HIV-suppressive factor released from CD8+ T cells[citation needed]. This chemokine has been localized to chromosome 17 in humans.[5]. RANTES was first identified in a search for genes expressed late (3-5 days) after T cell activation. It was subsequently determined to be a CC chemokine and expressed in more than 100 human diseases. RANTES expression is regulated in T lymphocytes by Kruppel like factor 13 (KLF13).[7][8][9][10] RANTES, along with the related chemokines MIP-1alpha and MIP-1beta, has been identified as a natural HIV-suppressive ...
Baggiolini M, Dahinden CA. CC chemokines in allergic inflammation. Immunol. Today (1994) 15:127-133.. Baggiolini M, Dewald B, Moser B. Interleukin-8 and related chemotactic cytokines-CXC and CC chemokines. Adv. Immunol. (1994) 55:97-179.. Barnes DA, Huston M, Holmes R, Benveniste EN, Yong VW, Scholz P, Perez HD. Induction of RANTES expression by astrocytes and astrocytoma cell lines. J. Neuroimmunol. (1996) 71: 207-214.. Beck LA, Dalke S, Leiferman KM, Bickel CA, Hamilton R, Rosen H, Bochner BS, Schleimer RP. Cutaneous injection of RANTES causes eosinophil recruitment: comparison of nonallergic and allergic human subjects. J Immunol. (1997) 159:2962-2972.. Bevilacqua MP, Gimbrone MA Jr. Inducible endothelial functions in inflammation and coagulation. Semin Thromb Hemost. (1987) 13:425-433.. Black RA, Rauch CT, Kozlosky CJ, Peschon JJ, Slack JL, Wolfson MF, Castner BJ, Stocking KL, Reddy P, Srinivasan S, Nelson N, Boiani N, Schooley KA, Gerhart M, Davis R, Fitzner, Johnson RS, Paxton RJ, March ...
Genomatix Software GmbH, Munich, Germany. The chemokine RANTES is produced by a variety of cell types in response to diverse stimuli. The molecular mechanisms involved in transcriptional control of RANTES can vary significantly between the various cells that express the gene and the specific activating stimuli used. For example, T cells strongly induce RANTES late (i.e. 3 to 7 days) after activation through their T cell receptor. Monocytes do not upregulate RANTES in response to TNF-alpha, IL-1beta or gamma-IFN, but quickly and transiently induce RANTES following stimulation with lipopolysaccaride (LPS) (maximal expression by 6 to 9 hours. By contrast, fibroblasts and astrocytes produce RANTES in response to TNF-alpha, IL-1 beta and gamma-IFN with the initial expression seen by 6 hours and maximal expression by 48 hours. The promoter region that regulates these diverse modes of expression may act as an enhancesome. It is compact, highly conserved over evolution, and can be efficiently studied ...
Tick-borne encephalitis virus (TBEV) is one of the most important flaviviruses that targets the central nervous system (CNS) and causes encephalitides in humans. Although neuroinflammatory mechanisms may contribute to brain tissue destruction, the induction pathways and potential roles of specific chemokines in TBEV-mediated neurological disease are poorly understood. BALB/c mice were intracerebrally injected with TBEV, followed by evaluation of chemokine and cytokine profiles using protein array analysis. The virus-infected mice were treated with the CC chemokine antagonist Met-RANTES or anti-RANTES mAb to determine the role of RANTES in affecting TBEV-induced neurological disease. The underlying signaling mechanisms were delineated using RANTES promoter luciferase reporter assay, siRNA-mediated knockdown, and pharmacological inhibitors in human brain-derived cell culture models. In a mouse model, pathological features including marked inflammatory cell infiltrates were observed in brain sections,
Chondrocytes produce RANTES and express RANTES receptors. RANTES and CCR5 were markedly increased in OA and after in vitro treatment of normal chondrocytes with IL-1. Chondrocyte activation and cartilage degradation were identified as novel biologic and pathogenetic activities of this chemokine.
Caroline Mouline, Guillaume Béranger, Heidy Schmid-Antomarchi, Danielle Quincey, David Momier, et al.. Monocytes differentiation upon treatment with a peptide corresponding to the C-terminus of activated T cell-expressed Tirc7 protein. Journal of Cellular Physiology, Wiley, 2012, 227 (8), pp.3088-3098. ⟨10.1002/jcp.23059⟩. ⟨hal-02404327⟩ ...
Dyer, AP; Mattick, C; Milnes, R; Gompels, UA; (2001) Novel beta herpes virus chemokine receptor shows rantes binding and transcriptional down regulation. [Conference or Workshop Item] Full text not available from this repository ...
MMP-1, MMP-3, and MMP-13 were expressed only in chondrocytes. The production of all MMPs was enhanced by contact coculture of chondrocytes with autologous T cells, whereas the production was not enhanced by separate coculture. Blockade of adhesion molecules had no influence on these responses. RANTES was expressed both in T cells and chondrocytes without stimulation. RANTES production was enhanced both in contact and in separate conditions only in OA samples, not in normal samples. ...
TY - JOUR. T1 - Differential effects of protein kinase C inhibitors on chemokine production in human synovial fibroblasts. AU - Jordan, Nicola J.. AU - Watson, Malcolm L.. AU - Yoshimura, Teizo. AU - Westwick, John. PY - 1996. Y1 - 1996. N2 - 1. Rheumatoid arthritis is associated with the accumulation and activation of selected populations of inflammatory cells within the arthritic joint. One putative signal for this process is the production, by resident cells, of a group of inflammatory mediators known as the chemokines. 2. The chemokines interleukin-8 (IL-8), monocyte chemotactic protein-1 (MCP-1) and RANTES (regulated on activation normal T-cell expressed and presumably secreted) are target-cell specific chemoattractants produced by synovial fibroblasts in response to stimulation with interleukin-1α (IL-1α) or tumour necrosis factor α (TNFα). The signalling pathways involved in their production are not well defined. We therefore used four different protein kinase C inhibitors to ...
We have demonstrated previously the potent activation of PLD by the chemokine IL-8 in T lymphocytes (18). We have now extended our findings to include the C-C chemokine RANTES in demonstrating that in the Jurkat T cell line, the activation of this enzyme occurs at subnanomolar concentrations and is dependent on the activation of small GTP-binding protein cofactors. RANTES-induced PLD activation is consistently maximal at 1 nM, a concentration corresponding to the optimal chemotaxis-inducing dose in normal T lymphocytes. Interestingly, PLD activation in T lymphocytes and Jurkat T cells appears to be an important biologic consequence of chemokine action and more readily measurable (at nanomolar concentrations) than readouts of receptor activation such as calcium flux. It was also apparent that RANTES is the only chemokine tested to date (RANTES, MIP-1α, MIP-1β, MCP-1, MCP-3, lymphotactin) that induces as robust a response as seen in this study, although the others listed were capable of low ...
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Ccl2 - Ccl2 (untagged) - Mouse chemokine (C-C motif) ligand 2 (Ccl2), (10ug) available for purchase from OriGene - Your Gene Company.
Human osteoclast formation from monocyte precursors under the action of receptor activator of nuclear factor-{kappa}B ligand (RANKL) was suppressed by granulocyte macrophage colony-stimulating factor (GM-CSF), with down-regulation of critical osteoclast-related nuclear factors. GM-CSF in the presence of RANKL and macrophage colony-stimulating factor resulted in mononuclear cells that were negative for tartrate-resistant acid phosphatase (TRAP) and negative for bone resorption. CD1a, a dendritic cell marker, was expressed in GM-CSF, RANKL, and macrophage colony-stimulating factor-treated cells and absent in osteoclasts. Microarray showed that the CC chemokine, monocyte chemotactic protein 1 (MCP-1), was profoundly repressed by GM-CSF. Addition of MCP-1 reversed GM-CSF suppression of osteoclast formation, recovering the bone resorption phenotype. MCP-1 and chemokine RANTES (regulated on activation normal T cell expressed and secreted) permitted formation of TRAP-positive multinuclear cells in the ...
title: RANTES gene promoter polymorphisms are associated with bronchial hyperresponsiveness in Korean children with asthma, doi: 10.1007/s00408-007-9049-3, category: Article
Authors: Reale, Marcella , Iarlori, Carla , Feliciani, Claudio , Gambi, Domenico Article Type: Research Article Abstract: Cerebral inflammation as well as systemic immunological alterations has been reported in Alzheimers disease (AD). We aimed to determine whether spontaneous and mitogen stimulated production of peripheral blood mononuclear cell (PBMC) cytokines, chemokines and chemokine receptors in clinically diagnosed patients with AD were unregulated. PBMC were purified from AD patients and from healthy controls. Supernatants were analyzed for cytokine levels by ELISA methods. mRNA expression was determined by RT-PCR. Expression of chemokine receptors CCR2 and CCR5 was determined by cytofluorimetric analysis. Both CCR5 and CCR2 expression were increased in AD patients respect to control subjects and the expression of CCR2 …and CCR5 was more frequent on CD4+ and less frequent on CD8+ cells. Levels of Th1-type cytokine IFNγ and chemokine RANTES were increased and levels of Th2-type ...
For several years, it has been known that stimulation with bacterial LPS protects macrophages from productive infection by HIV-1 in vitro ((15), (16)). Despite the potential implications of this finding for the pathogenesis and treatment of HIV infection, the mechanisms responsible for the HIV suppressive effect of LPS have remained unknown. Our present results indicate that LPS stimulates human MDM to release soluble factors, the C-C chemokines RANTES, MIP-1α, and MIP-1β, that strongly inhibit HIV replication, not only in macrophages but also in T lymphocytes.. These data may help redefine our current understanding of the role played by monocyte/macrophages in the pathogenesis of HIV infection. Macrophages have been viewed mostly negatively, as major targets for infection ((3), (4)), reservoirs for the virus ((1), (2)), triggers for T cell apoptosis ((36), (37)), and last but not least, as a source of soluble factors (TNF-α, IL-1, IL-6) that sustain viral replication ((27), (38), (39)). The ...
Chemokine (C-C motif) ligand 8 (CCL8), also known as monocyte chemoattractant protein 2 (MCP2), is a protein that in humans is encoded by the CCL8 gene. CCL8 is a small cytokine belonging to the CC chemokine family. The CCL8 protein is produced as a precursor containing 109 amino acids, which is cleaved to produce mature CCL8 containing 75 amino acids. The gene for CCL8 is encoded by 3 exons and is located within a large cluster of CC chemokines on chromosome 17q11.2 in humans. MCP-2 is chemotactic for and activates many different immune cells, including mast cells, eosinophils and basophils, (that are implicated in allergic responses), and monocytes, T cells, and NK cells that are involved in the inflammatory response. CCL8 elicits its effects by binding to several different cell surface receptors called chemokine receptors. These receptors include CCR1, CCR2B and CCR5. CCL8 is a CC chemokine that utilizes multiple cellular receptors to attract and activate human leukocytes. CCL8 is a potent ...
Using thapsigargin (Tg), an agent that mobilizes calcium by directly emptying intracellular stores, we previously showed that intracellular calcium may play an important role in the regulation of intercellular adhesion molecule (ICAM)-1 gene expression induced by cytokines in human airway smooth muscle (ASM) cells. In the present study, we extended this previous observation by comparing the effect of Tg and other calcium-mobilizing G-protein-coupled receptor (GPCR) agonists on the expression of different pro-inflammatory genes in response to tumor necrosis factor (TNF)-alpha in ASM cells. We found that in resting cells, Tg (10-100 nM) or the bradykinin (BK) (1-10 muM) and thrombin (Thr) (1 U/ml) stimulated interleukin (IL)-6 secretion but had no effect on regulated on activation, normal T cells expressed and secreted (RANTES) levels. More importantly, such calcium-mobilizing agents significantly enhanced TNF-alpha-induced IL-6 secretion while RANTES secretion was abrogated. The use of ...
Chemokine (C-C motif) ligand 8--also known as monocyte chemoattractant protein 2 (MCP-2), HC14, SCYA8, or SCYA10--is a protein encoded by the CCL8 gene. The precursor protein (109 amino acids) is cleaved to produce mature CCL8 (75 amino acids). CCL8 activates many different immune cells, including mast cells, eosinophils, and basophils (implicated in allergic responses), and monocytes, T cells, and NK cells (involved in the inflammatory response). CCL8 acts through binding to several different cell surface chemokine receptors, including CCR1, CCR2B, and CCR5 (one of the major co-receptors for HIV-1).. ...
The contribution of inflammation to the development of fibrosis varies in different conditions, and understanding the interaction between these processes is relevant to devise therapeutic strategies for chronic diseases such as pancreatitis. Identification of the chemokine system has elucidated the molecular mechanisms regulating leucocyte trafficking in a given tissue. Chemokines are a family of small cytokines that exert gradient dependent chemoattraction of cells bearing specific cognate receptors. The chemokine system is considerably complex, as indicated by the high number of ligands and receptors, and by the fact that the same chemokine may bind more than one receptor and the same receptor more than one chemokine.2 Additionally, the effects of chemokines are not limited to inflammation as the majority of cells express at least one chemokine receptor. A related aspect of chemokine biology is the distinction between homeostatic and inflammatory chemokines, where expression of the latter ...
In vitro replication of SIVcpz is suppressed by beta-chemokines and CD8+ T cells but not by natural killer cells of infected chimpanzees ...
Primary infections of the human cytomegalovirus (HCMV) are followed by a lifelong infection in the state of latency or persistence. It is believed that the virus employs a number of immunomodulatory mechanisms to establish latent infections. Among these are the inhibition of cytotoxic CD8+ T-cells by US11 and the impairment of leukocyte migration by US28. The potency of US11 to mediate the inhibition of T-cell activation was analysed in a model of MHC class I mediated T-cell activation. Surface expression of MHC class I molecules was reduced by 60 % after expression of US11 in murine dendritic cells. In contrast, there was no reduction in the capacity of the dendritic cells to induce T-cell proliferation. The US28 gene product has been characterized as a functional receptor for the inflammatory chemokines RANTES, MCP-1, MCP-3, MIP-1?? MIP-1? and fractalkine.Upon ligand stimulation US28 mediates the activation of MAPK and additionally a constitutive activation of NF-?B. By generating site ...
AYOXXA launches LUNARISTM Human and Mouse Chemokine Kits to explore chemokine signaling LUNARISTM Chemokine Kits are validated for the quantitative analysis of
When two chemokine receptors in the brain interact, leukemic cells (stained green) creep out of a small vein in the membrane covering the brain of a mouse and enter the cerebrospinal fluid. The chemokine CCL19, which is in the endothelium lining the vein, is stained blue in this immunofluorescent image.
In the present study, we sought to examine the molecular basis for the differential regulation of several members of the IFN-α/β gene family (IFNA and IFNB) by IRF-3 and IRF-7. The IFNB, IFNA1, IFNA2, and RANTES promoters were activated by coexpression of either IRF-3 or IRF-7, whereas the IFNA4, IFNA7, and IFNA14 promoters were exclusively activated by IRF-7 and not by IRF-3. Analysis of protein-DNA interactions revealed that recombinant IRF-3 and IRF-7 selectively bound to different regions of the IFNB promoter; IRF-3 bound preferentially to the PRDIII domain of the IFNB promoter, while IRF-7 interacted exclusively with the PRDI domain. PCR-mediated DNA binding site selection results demonstrated that IRF-3 recognized the IRF consensus element 5′-GAAANNGAAANN-3′. Replacement of a single nucleotide within the GAAA core half-site was sufficient to preclude IRF-3 DNA binding. IRF-7 bound to a related sequence motif but with greater flexibility than IRF-3; a single nucleotide replacement did ...
Looking for online definition of C-C motif chemokine 2 in the Medical Dictionary? C-C motif chemokine 2 explanation free. What is C-C motif chemokine 2? Meaning of C-C motif chemokine 2 medical term. What does C-C motif chemokine 2 mean?
Chemokine (C-C motif) ligand 8--also known as monocyte chemoattractant protein 2 (MCP-2), HC14, SCYA8, or SCYA10--is a protein encoded by the CCL8 gene. The precursor protein (109 amino acids) is cleaved to produce mature CCL8 (75 amino acids). CCL8 activates many different immune cells, including mast cells, eosinophils, and basophils (implicated in allergic responses), and monocytes, T cells, and NK cells (involved in the inflammatory response). CCL8 acts through binding to several different cell surface chemokine receptors, including CCR1, CCR2B, and CCR5 (one of the major co-receptors for HIV-1).. ...
Co-Author, The Evidence of Things Not Seen: Non-Matches as Evidence of Innocence, 98 Iowa L. Rev. 577 (2013). Co-Author, Toll-like receptor 7 is required for effective adaptive immune responses that prevent persistent virus infection, Cell Host Microbe., 2012 Jun.. Angelosanto JM, Blackburn SD, Crawford A, Wherry EJ, Progressive loss of memory T cell potential and commitment to exhaustion during chronic viral infection. J Virol., 2012 Aug.. Crawford A, Angelosanto JM, Nadwodny KL, Blackburn SD, Wherry EJ, A role for the chemokine RANTES in regulating CD8 T cell responses during chronic viral infection. PLoS Pathog., 2011 Jul.. Blackburn SD, et al., Tissue-specific differences in PD-1 and PD-L1 expression during chronic viral infection: implications for CD8 T-cell exhaustion. J Virol., 2010 Feb.. Shin H, Blackburn SD, et al., A role for the transcriptional repressor Blimp-1 in CD8(+) T cell exhaustion during chronic viral infection. Immunity, 2009 Aug.. Blackburn SD, et al. Co-regulation of CD8 T ...
Previously, we showed that a chemokine CCL2 recruits IMs to metastatic sites where they differentiate to MAMs (Qian et al., 2011). In this study, we revealed a novel role for CCL2 as a trigger of a prometastatic chemokine cascade involving CCL3 signaling via CCR1 that is required for efficient metastasis. These data illustrate a signaling relay that amplifies the pathology already in the system by promoting retention of recruited monocytes that stimulate tumor cell establishment at the metastatic site.. Our in vivo and in vitro results indicate that CCL2 can increase CCL3 expression in MAMs at the metastasis site. The CCL2-induced CCL3 expression is likely to be specific to the prometastatic macrophage lineage, as neutralization of CCL2 by antibodies significantly reduced Ccl3 expression in IMs and MAMs, but not in resident monocytes or macrophages. Consistent with this interpretation, expression of Ccl3 was highest in MAMs compared with other leukocytes in the tumor-bearing lung. Importantly, a ...
Emeson, E E., Bcg and c. Parvum enhance selective recruitment of specifically reactive t-lymphocytes. Abstr. (1977). Subject Strain Bibliography 1977. 2521 ...
The chemokine (C-C motif) ligand 2 (CCL2) is also referred to as monocyte chemoattractant protein 1 (MCP1) and small inducible cytokine A2. CCL2 is a small cytokine that belongs to the CC chemokine family. CCL2 recruits monocytes, memory T cells, and dendritic cells to the sites of inflammation produced by either tissue injury or infection ...
The therapeutic goal in autoimmune diseases such as RA is to control disease, to establish remission, and eventually to cure. In theory, this goal can be achieved using either Ag-specific approaches, for example, elimination of self-reactive T cells (assuming that a finite number of key Ags can be identified as the target of the autoimmune process in RA), or the non-Ag-specific approaches, for example, blockade of cytokines as in the case of TNF-a neutralization. Currently, only the latter types of approaches have yielded clinical benefit, and it is in this category that approaches to block chemokines or receptors may be included. Despite their appeal in terms of effectiveness, non-Ag-specific approaches carry a higher risk of immunosuppression and opportunistic infections (48).. Although there is a myriad of ongoing clinical trials testing the effects of chemokine/receptor blockers in RA (Table 1), to date one cannot yet predict how many of the current targets will prove to be clinically ...
Reaktivität: Meerschweinchen - Probe: Serum, Cell Culture Supernatant. | Chemokine (C-C Motif) Ligand 8 (CCL8) ELISA Kit (ABIN628807).
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Mouse C-C Motif Chemokine 2 / Monocyte Chemoattractant Protein 1 (CCL2/MCP1) standard, for use in running standard curves in AlphaLISA no-wash detection assays.
Kemokiinid (ka kemotaktsed tsütokiinid; inglise keeles chemokines) on selgroogsete loomade mitmete tuumaga rakkude poolt (eosinofiilid, basofiilid, neutrofiilid, makrofaagid, endoteelirakud, keratinotsüüdid, fibroblastid jt) komplekteeritavate ja vabastatavate selliste väikesemolekuliliste looduslike valkude perekond, mis vahendavad lühiajaliselt ja lokaalselt erinevaid bioloogilisi toimeid ja rakkudevahelist informatsiooni seondudes G-valguga seotud retseptoreid omavate rakkude membraaniga ja aktiveerides ensüümi fosfolipaas C. Kemokiinide sarnaseid valke on tuvastatud teatud bakteritel ja viirustel. Kemokiinide funktsiooniks on mitmete rakkude sundviimine nakkus- või põletikukoldesse, lisaks reguleerivad kemokiinid lümfikudede ja närvisüsteemi arengut ja leukotsüütide migratsiooni, küpsemist, aktivatsiooni jm. Varem on neid liigitatud α,β,γ ja δ- rühma, tänapäeval liigitatakse aga sellisteks perekondadeks nagu CC- (β-kemokiinid), CXC- (α-kemokiinid), CX3C- (δ- ...
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