scholarly journals Adenosine inhibits cytosolic calcium signals and chemotaxis in hepatic stellate cells

2007 ◽  
Vol 292 (1) ◽  
pp. G395-G401 ◽  
Author(s):  
Ardeshir Z. Hashmi ◽  
Wyel Hakim ◽  
Emma A. Kruglov ◽  
Azuma Watanabe ◽  
William Watkins ◽  
...  
Keyword(s):  
Tissue Injury ◽  
Stellate Cell ◽  
Cellular Responses ◽  
Cytosolic Calcium ◽  
Collagen I ◽  
Dependent Manner ◽  
Activation Markers ◽  
Cellular Hypoxia ◽  
Dose Dependent ◽  
Transwell System

Adenosine is produced during cellular hypoxia and apoptosis, resulting in elevated tissue levels at sites of injury. Adenosine is also known to regulate a number of cellular responses to injury, but its role in hepatic stellate cell (HSC) biology and liver fibrosis is poorly understood. We tested the effect of adenosine on the cytosolic Ca2+ concentration, chemotaxis, and upregulation of activation markers in HSCs. We showed that adenosine did not induce an increase in the cytosolic Ca2+ concentration in LX-2 cells and, in addition, inhibited increases in the cytosolic Ca2+ concentration in response to ATP and PDGF. Using a Transwell system, we showed that adenosine strongly inhibited PDGF-induced HSC chemotaxis in a dose-dependent manner. This inhibition was mediated via the A2a receptor, was reversible, was reproduced by forskolin, and was blocked by the adenylate cyclase inhibitor 2,5-dideoxyadenosine. Adenosine also upregulated the production of TGF-β and collagen I mRNA. In conclusion, adenosine reversibly inhibits Ca2+ fluxes and chemotaxis of HSCs and upregulates TGF-β and collagen I mRNA. We propose that adenosine provides 1) a “stop” signal to HSCs when they reach sites of tissue injury with high adenosine concentrations and 2) stimulates transdifferentiation of HSCs by upregulating collagen and TGF-β production.

Lenalidomide Strongly Enhances Natural Killer (NK) Cell Mediated Antibody-Dependent Cellular Cytotoxicity (ADCC) of Rituximab Treated Non-Hodkin’s Lymphoma Cell Lines In Vitro.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3714-3714 ◽  
Author(s):  
Lei Wu ◽  
Peter Schafer ◽  
George Muller ◽  
David Stirling ◽  
J. Blake Bartlett
Keyword(s):  
Nk Cells ◽  
Tumor Cells ◽  
Cell Lines ◽  
Nk Cell ◽  
Dependent Manner ◽  
Activation Markers ◽  
Early Results ◽  
Ifn Γ ◽  
Dose Dependent

Abstract Lenalidomide (Revlimid® is approved for the treatment of transfusion-dependent patients with anemia due to low- or intermediate-1-risk MDS associated with a del 5q cytogenetic abnormality with or without additional cytogenetic abnormalities, and in combination with dexamethasone is for the treatment of multiple myeloma patients who have received at least one prior therapy. Encouraging early results suggest a potential for clinical efficacy in B cell non-Hodgkin’s lymphoma (NHL). Potential mechanisms of action include anti-angiogenic, anti-proliferative and immunomodulatory activities. Lenalidomide has been shown to enhance Th1-type cytokines and T cell and NK cell activation markers in patients with advanced cancers. Furthermore, lenalidomide has been shown to enhance rituximab-mediated protection in a SCID mouse lymphoma model in vivo. We have utilized an in vitro ADCC system to assess the ability of lenalidomide to directly enhance human NK cell function in response to therapeutic antibodies, such as rituximab (chimeric anti-CD20 mAb). Isolated NK cells produced little or no IFN-γ in response to IgG and/or IL-2 or IL-12. However, pre-treatment of NK cells with lenalidomide greatly enhanced IFN-γ production by NK cells in a dose-dependent manner. In a functional ADCC assay, NHL cell lines (Namalwa, Farage & Raji) were pre-coated with rituximab and exposed to NK cells pre-treated with lenalidomide in the presence of either exogenous IL-2 or IL-12. After 4 hours in culture the viability of the tumor cells was assessed. Lenalidomide consistently and synergistically increased the killing of tumor cells in a dose-dependent manner and up to >4-fold compared to rituximab alone. Rituximab alone had only a small effect in this model and there was no killing of cells in the absence of rituximab. The presence of either exogenous IL-2 or IL-12 was required to see enhanced killing by lenalidomide. In cancer patients lenalidomide has been shown to increase serum IL-12 levels and is also known to induce IL-2 production by T cells in vitro. Potential mechanisms for enhanced ADCC include increased signaling through NK FCγ receptors and/or IL-2 or IL-12 receptors. However, we found that these receptors are unaffected by lenalidomide, although downstream effects on NK signaling pathways are likely and are being actively investigated. In conclusion, we have shown that lenalidomide strongly enhances the ability of rituximab to induce ADCC mediated killing of NHL cells in vitro. This provides a strong rationale for combination of these drugs in patients with NHL and CLL.

scholarly journals Ionizing radiation augments glioma tropism of mesenchymal stem cells

2018 ◽  
Vol 128 (1) ◽  
pp. 287-295 ◽  
Author(s):  
Jonathan G. Thomas ◽  
Brittany C. Parker Kerrigan ◽  
Anwar Hossain ◽  
Joy Gumin ◽  
Naoki Shinojima ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Ionizing Radiation ◽  
Nude Mice ◽  
Tissue Injury ◽  
Statistical Significance ◽  
Dependent Manner ◽  
Weak Attractor ◽  
Dose Dependent

OBJECTIVEMesenchymal stem cells (MSCs) have been shown to localize to gliomas after intravascular delivery. Because these cells home to areas of tissue injury, the authors hypothesized that the administration of ionizing radiation (IR) to tumor would enhance the tropism of MSCs to gliomas. Additionally, they sought to identify which radiation-induced factors might attract MSCs.METHODSTo assess the effect of IR on MSC migration in vitro, transwell assays using conditioned medium (CM) from an irradiated commercially available glioma cell line (U87) and from irradiated patient-derived glioma stem-like cells (GSCs; GSC7-2 and GSC11) were employed. For in vivo testing, green fluorescent protein (GFP)-labeled MSCs were injected into the carotid artery of nude mice harboring orthotopic U87, GSC7-2, or GSC17 xenografts that were treated with either 0 or 10 Gy of IR, and brain sections were quantitatively analyzed by immunofluorescence for GFP-positive cells. These GSCs were used because GSC7-2 is a weak attractor of MSCs at baseline, whereas GSC17 is a strong attractor. To determine the factors implicated in IR-induced tropism, CM from irradiated GSC7-2 and from GSC11 was assayed with a cytokine array and quantitative ELISA.RESULTSTranswell migration assays revealed statistically significant enhanced MSC migration to CM from irradiated U87, GSC7-2, and GSC11 compared with nonirradiated controls and in a dose-dependent manner. After their intravascular delivery into nude mice harboring orthotopic gliomas, MSCs engrafted more successfully in irradiated U87 (p = 0.036), compared with nonirradiated controls. IR also significantly increased the tropism of MSCs to GSC7-2 xenografts (p = 0.043), which are known to attract MSCs only poorly at baseline (weak-attractor GSCs). Ionizing radiation also increased the engraftment of MSCs in strong-attractor GSC17 xenografts, but these increases did not reach statistical significance. The chemokine CCL2 was released by GSC7-2 and GSC11 after irradiation in a dose-dependent manner and mediated in vitro transwell migration of MSCs. Immunohistochemistry revealed increased CCL2 in irradiated GSC7-2 gliomas near the site of MSC engraftment.CONCLUSIONSAdministering IR to gliomas enhances MSC localization, particularly in GSCs that attract MSCs poorly at baseline. The chemokine CCL2 appears to play a crucial role in the IR-induced tropism of MSCs to gliomas.

scholarly journals An Analytic Contemplation of the Conspicuous Vicissitudes in the Histomorphology of Corpuscles of Stannius of a Freshwater CatfishMystus tengara(Hamilton, 1822) due to the Exposure of ZnS Nanoparticles

Scientifica ◽  
2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Nilanjana Chatterjee ◽  
Baibaswata Bhattacharjee
Keyword(s):  
Cellular Responses ◽  
Dependent Manner ◽  
Cell Type ◽  
Defence Mechanism ◽  
Organ Function ◽  
Zns Nanoparticles ◽  
Corpuscles Of Stannius ◽  
Granular Cytoplasm ◽  
Enhanced Surface ◽  
Dose Dependent

Enhanced surface photooxidation property associated with the ZnS nanoparticles caused the reduction of dissolved oxygen content in water in a dose dependent manner, when ZnS nanoparticles of different sizes are exposed to the water in various concentrations. This property was more prominent for ZnS nanoparticles with smaller sizes.Mystus tengara, exposed to ZnS nanoparticles, responded to hypoxia with varied behavioural, physiological, and cellular responses in order to maintain homeostasis and organ function in an oxygen-depleted environment. The histomorphology of corpuscles of Stannius of the fish showed conspicuous vicissitudes under exposure of ZnS nanoparticles. The population of the cell type with granular cytoplasm showed significant increase at the expense of the other that consisted of agranular cytoplasm with increasing nanoparticle concentration. This can be explained as the defence mechanism of the fish against ZnS nanoparticle induced hypoxia and environmental acidification. The altering histomorphology has been studied employing an analytical approach.

scholarly journals Interaction with Mesenchymal Stem Cells Provokes Natural Killer Cells for Enhanced IL-12/IL-18-Induced Interferon-Gamma Secretion

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Heike Thomas ◽  
Marcus Jäger ◽  
Katharina Mauel ◽  
Sven Brandau ◽  
Sara Lask ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Nk Cells ◽  
Natural Killer ◽  
Tissue Regeneration ◽  
Tissue Injury ◽  
Cell Contact ◽  
Dependent Manner ◽  
Close Proximity ◽  
Dose Dependent

Tissue injury induces an inflammatory response accompanied by the recruitment of immune cells and of mesenchymal stem cells (MSC) that contribute to tissue regeneration. After stimulation with interleukin- (IL-) 12 and IL-18 natural killer (NK) cells secrete the proinflammatory cytokine interferon- (IFN-)γ. IFN-γplays a crucial role in the defense against infections and modulates tissue regeneration. In consideration of close proximity of NK cells and MSC at the site of injury we investigated if MSC could influence the ability of NK-cells to produce IFN-γ. Coculture experiments were performed with bone marrow-derived human MSC and human NK cells. MSC enhanced the ability of IL-12/IL-18-stimulated NK cells to secrete IFN-γin a dose-dependent manner. This activation of NK cells was dependent on cell-cell contact as well as on soluble factors. The increased IFN-γsecretion from NK cells after contact with MSC correlated with an increased level of intracellular IFN-γ. Alterations in the IL-12 signaling pathway including an increased expression of the IL-12β1 receptor subunit and an increased phosphorylation of signal transducer and activator of transcription 4 (STAT4) could be observed. In conclusion, MSC enhance the IFN-γrelease from NK cells which might improve the defense against infections at the site of injury but additionally might affect tissue regeneration.

scholarly journals Choline-Sigma-1R as an Additional Mechanism for Potentiation of Orexin by Cocaine

2021 ◽  
Vol 22 (10) ◽  
pp. 5160
Author(s):  
Jeffrey L. Barr ◽  
Pingwei Zhao ◽  
G. Cristina Brailoiu ◽  
Eugen Brailoiu
Keyword(s):  
Nucleus Accumbens ◽  
Calcium Concentration ◽  
Critical Role ◽  
Cytosolic Calcium ◽  
Dependent Manner ◽  
Ip3 Receptors ◽  
Orexin A ◽  
Signaling Mechanism ◽  
Orexin Receptors ◽  
Dose Dependent

Orexin A, an endogenous peptide involved in several functions including reward, acts via activation of orexin receptors OX1 and OX2, Gq-coupled GPCRs. We examined the effect of a selective OX1 agonist, OXA (17-33) on cytosolic calcium concentration, [Ca2+]i, in neurons of nucleus accumbens, an important area in the reward circuit. OXA (17-33) increased [Ca2+]i in a dose-dependent manner; the effect was prevented by SB-334867, a selective OX1 receptors antagonist. In Ca2+-free saline, the OXA (17-33)-induced increase in [Ca2+]i was not affected by pretreatment with bafilomycin A1, an endo-lysosomal calcium disrupter, but was blocked by 2-APB and xestospongin C, antagonists of inositol-1,4,5-trisphosphate (IP3) receptors. Pretreatment with VU0155056, PLD inhibitor, or BD-1047 and NE-100, Sigma-1R antagonists, reduced the [Ca2+]i response elicited by OXA (17-33). Cocaine potentiated the increase in [Ca2+]i by OXA (17-33); the potentiation was abolished by Sigma-1R antagonists. Our results support an additional signaling mechanism for orexin A-OX1 via choline-Sigma-1R and a critical role for Sigma-1R in the cocaine–orexin A interaction in nucleus accumbens neurons.

The role of intracellular Ca2+ during early sexual development in Dictyostelium discoideum: effects of LaCl3, LaCl3, Ins(1,4,5)P3, TMB-8, chlortetracycline and A23187 on cell fusion

1988 ◽  
Vol 90 (3) ◽  
pp. 465-473 ◽  
Author(s):  
MICHAEL A. LYDAN ◽  
DANTON H. O'DAY
Keyword(s):  
Dictyostelium Discoideum ◽  
Cell Fusion ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Ionophore A23187 ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Extracellular Environment ◽  
Internal Calcium

The agents LaCl3, Ins(1,4,5)P3, TMB-8, chlortetracycline (CTC) and A23187 were used to study the requirement for internal calcium mobilization during gamete cell fusion in Dictyostelium discoideum. The inhibition of the influx of calcium (LaCl3) prevented cell fusion in a dose-dependent manner. At the intracellular level, Ins(1,4,5)P3, an endogenous regulator of calcium release from intracellular stores, stimulated cell fusion within one hour following its addition. Treatment with agents that prevent the release of calcium from intracellular stores (TMB-8, CTC) also inhibited cell fusion in a dose-dependent manner. However, the non-specific augmentation of cytosolic calcium levels through the use of the ionophore A23187 inhibited cell fusion, and the amount inhibition was directly related to the drug concentration. Studies on cell morphology and growth plus results from reversibility experiments involving the ability to form macrocysts reveal that these effects are not due to non-specific drug toxicity. In total, these results suggest that the mobilization of calcium both from the extracellular environment and from intracellular stores important and is probably regulated during gamete cell fusion in D. discoideum.

Dexamethasone Reduces Viability of Bone Marrow Derived Macrophages

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 4732-4732
Author(s):  
Yasmin Ohana ◽  
Miriam C Souroujon ◽  
Moshe Mittelman ◽  
Drorit Neumann
Keyword(s):  
Bone Marrow ◽  
Clinical Implications ◽  
Dependent Manner ◽  
Activated Macrophages ◽  
Activation Markers ◽  
Inflammatory Protein ◽  
Dose Dependent ◽  
Macrophage Inflammatory Protein ◽  
Mrna Expression Levels ◽  
Apoptotic Mechanism

Abstract Abstract 4732 Glucocorticoids are steroid hormones with pleotropic effects and are widely used in clinical practice. Glucocorticoids affect almost every cell of the immune system. Here, we show that dexamethasone (DEX), a synthetic glucocorticoid, decreases viability of naïve bone marrow-derived macrophages (BMDM) in a dose dependent manner. A 24-hour incubation with 0.1, 0.5 and 1 microM DEX reduced BMDM viability by 22%, 26% and 34%, respectively, compared with untreated cells. Annexin-PI staining suggests an apoptotic mechanism. Administration of DEX in the presence of lipopolysaccharide (LPS) protected the BMDM against DEX-mediated cell death. In addition to its effect on cell viability, DEX also significantly reduced the percentage of BMDM expressing high levels of the differentiation and activation markers F4/80 and CD11b (5 fold decrease mediated by 1 microM DEX). Treatment of BMDM with 1 microM DEX also led to a ∼ 50% decrease in macrophage inflammatory protein 1 alpha (MIP-1-alpha) mRNA expression levels. These findings may contribute to a better understanding of DEX effects on naïve and activated macrophages and may have clinical implications in various diseases, including infection, inflammation and neoplastic diseases. Glucocorticoids are steroid hormones with pleotropic effects and are widely used in clinical practice. Glucocorticoids affect almost every cell of the immune system. Here, we show that dexamethasone (DEX), a synthetic glucocorticoid, decreases viability of naïve bone marrow-derived macrophages (BMDM) in a dose dependent manner. A 24-hour incubation with 0.1, 0.5 and 1 microM DEX reduced BMDM viability by 22%, 26% and 34%, respectively, compared with untreated cells. Annexin-PI staining suggests an apoptotic mechanism. Administration of DEX in the presence of lipopolysaccharide (LPS) protected the BMDM against DEX-mediated cell death. In addition to its effect on cell viability, DEX also significantly reduced the percentage of BMDM expressing high levels of the differentiation and activation markers F4/80 and CD11b (5 fold decrease mediated by 1 microM DEX). Treatment of BMDM with 1 microM DEX also led to a ∼ 50% decrease in macrophage inflammatory protein 1 alpha (MIP-1-alpha) mRNA expression levels. These findings may contribute to a better understanding of DEX effects on naïve and activated macrophages and may have clinical implications in various diseases, including infection, inflammation and neoplastic diseases.v Disclosures: No relevant conflicts of interest to declare.

Arginine vasopressin stimulates H+-ATPase in MDCK cells via V1 (cell Ca2+) and V2 (cAMP) receptors

2004 ◽  
Vol 286 (2) ◽  
pp. F402-F408 ◽  
Author(s):  
Maria Oliveira-Souza ◽  
Raif Musa-Aziz ◽  
Gerhard Malnic ◽  
Margarida de Mello Aires
Keyword(s):  
Arginine Vasopressin ◽  
Mdck Cells ◽  
Specific Inhibitor ◽  
Cytosolic Calcium ◽  
Dependent Manner ◽  
Madin Darby Canine Kidney ◽  
Dose Dependent ◽  
Darby Canine Kidney ◽  
Canine Kidney ◽  
Stimulation Of

The effect of arginine vasopressin (AVP) and/or atrial natriuretic peptide (ANP) on the regulation of intracellular pH (pHi) via H+-ATPase and of cytosolic calcium ([Ca2+]i) was investigated in Madin-Darby canine kidney (MDCK) cells by the fluorescent probes BCECF-AM and fluo-4-AM, respectively. The pHi recovery rate was examined after intracellular acidification following an NH4Cl pulse, in the presence of zero Na+ plus Schering 28080 (a specific inhibitor of H+-K+-ATPase). AVP (10-12-10-6 M) increased the rate of pHi recovery and [Ca2+]i in a dose-dependent manner. V1- or V2-receptor antagonists impaired the effect of AVP on both processes, and DDAVP (10-12-10-6 M; a V2-selective agonist) caused a dose-dependent stimulation of them. [Ca2+]i or cAMP (as increased by 10-5 M thapsigargin or 8-BrcAMP, respectively) alone had no effect on H+-ATPase, but their synergic action was necessary to stimulate H+-ATPase. In agreement with these findings, ANP (10-6 M) or dimethyl-BAPTA-AM (5 × 10-5 M), impairing the increase of [Ca2+]i in response to AVP, blocks the stimulatory effect of AVP on H+-ATPase.

Escitalopram Impairs Thrombin-Induced Platelet Response, Cytoskeletal Assembly and Activation of Associated Signalling Pathways

2017 ◽  
Vol 117 (12) ◽  
pp. 2312-2321 ◽  
Author(s):  
Irene Lopez-Vilchez ◽  
Didac Jerez-Dolz ◽  
Maribel Diaz-Ricart ◽  
Victor Navarro ◽  
M. Urooj Zafar ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Platelet Aggregation ◽  
Statistical Significance ◽  
Ultrastructural Changes ◽  
Signalling Pathways ◽  
Dependent Manner ◽  
Platelet Response ◽  
Activation Markers ◽  
Irreversible Aggregation ◽  
Dose Dependent

Background Serotonin reuptake inhibitors (SSRIs) may impair platelet function. Thrombin is a strong platelet agonist causing irreversible aggregation, release of granules' contents, cytoskeletal rearrangement and activation of signalling pathways. We investigated the effects of the SSRI escitalopram (SCIT) on thrombin-induced platelet response. Methods Isolated platelets were exposed to SCIT and activated with thrombin. We evaluated (1) platelet response by aggregometry and flow cytometry; (2) modifications in cytoskeleton proteins and signalling pathways by electrophoresis and Western blot; and (3) ultrastructural changes in platelets by electron microscopy. Results SCIT inhibited platelet response to thrombin, measured as platelet aggregation and expression of activation markers CD62-P and CD63 from platelet granules. Platelet aggregation decreased in a dose-dependent manner, reaching statistical significance with SCIT ≥32 µg/mL (65.4 ± 6.8% vs. 77.7 ± 2.5% for controls; p < 0.05). Expression of activation markers was statistically reduced with SCIT ≥20 µg/mL (p < 0.05). SCIT impaired the polymerization of the actin cytoskeleton and association of contractile proteins during activation with thrombin (p < 0.05 with SCIT ≥50 µg/mL). Resting platelets incubated with SCIT became most spherical, with increased platelet roundness (p < 0.01, SCIT 50 µg/mL vs. control). SCIT interfered with signalling pathways modulated by thrombin (RhoA, PKC, Erk1/2 and PI3K/AKT). Conclusions Our data indicate that SCIT inhibits thrombin-induced platelet response and interferes with cytoskeletal assembly and related signalling pathways, thus resulting in compromised release of granules' contents, reduced platelet activation and aggregation. These mechanisms may explain the antithrombotic benefits observed in patients treated with this SSRI, and could become new therapeutic targets for future antithrombotic strategies.

Immune Effects of Imatinib in Chronic Myelogenous Leukemia In Vitro.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2956-2956
Author(s):  
Dagmar Bund ◽  
Raymund Buhmann ◽  
Hans-Jochem Kolb
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Myelogenous Leukemia ◽  
Dependent Manner ◽  
Activation Markers ◽  
Antigen Presenting ◽  
Dose Dependent

Abstract Imatinib mesylate, a potent and selective inhibitor of the BCR-ABL tyrosine kinase, has been shown to induce durable haematological and major cytogenetic responses in a high percentage of CML patients. However in most patients the disease recurs, when imatinib is discontinued. In contrast, allogeneic stem cell transplantation (ASCT) is considered to be curative by the immune effect of donor T cells against CML progenitor cells. In this context, the role of imatinib is controversial; it may improve the results of ASCT by reducing the tumour load, it may also reduce the effect of donor lymphocyte transfusions (DLT) by impairing the function of T cells and the capacity of myeloid cells to present antigen. Patient derived CML-cells were studied for the stimulation of allogeneic HLA-matched and mismatched T-cells in the presence and absence of imatinib. In a 5 day culture the proliferative response of HLA-mismatched T cells was evaluated in presence of different concentrations of imatinib (0, 1, 2, or 5 micro M) and various responder-to-stimulator ratios. Thereby, proliferation was detected via a CFDA based assays and the activation profile (CD25, CD69) of the T-cells was determined by FACS. Cr51-release assays were performed after a 7 day culture of CML cells with HLA-matched T cells to test cytotoxicity of CD8+ T-cells. In addition, we characterized the antigen-presenting profile (CD14, CD33, HLA-DR, CD40, CD80, CD86, CD54, CD58) of the CML cells over a 5 day culture with and without imatinib. The presence of imatinib inhibited the proliferative capacity of allogeneic T-cells in a dose-dependent manner. Also, the expression of T cell activation markers was reduced in the presence of the different imatinib concentrations. Preincubation of CML cells with imatinib for 48 hours strengthened the effect on proliferation and activation of T cells. Moreover, imatinib impaired the cytotoxic function of T-cell (HLA-matched setting; CR51-release assay) also in a dose-dependent manner. Finally, the antigen-presenting profile of the myeloid leukemia cells was down regulated by increasing concentrations of imatinib. In summary, imatinib may interfere with the T cellular immune response and the antigen presenting profile on the CML cells in vitro. These results may have an impact on new strategies of treatment of CML with immunotherapy.

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