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[PMID]: 25680810
[Au] Autor:Park JY; Shin DJ; Lee SH; Lee JJ; Suh GH; Cho D; Kim SK
[Ad] Address:Department of Companion & Laboratory Animal Science, Kongju National University, Yesan, Chungnam 340-702, Republic of Korea....
[Ti] Title:The anti-canine distemper virus activities of ex vivo-expanded canine natural killer cells.
[So] Source:Vet Microbiol;176(3-4):239-49, 2015 Apr 17.
[Is] ISSN:1873-2542
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Natural killer (NK) cells play critical roles in induction of antiviral effects against various viruses of humans and animals. However, few data on NK cell activities during canine distemper virus (CDV) infections are available. Recently, we established a culture system allowing activation and expansion of canine non-B, non-T, large granular NK lymphocytes from PBMCs of normal dogs. In the present study, we explored the ability of such expanded NK cells to inhibit CDV infection in vitro. Cultured CD3(-)CD5(-)CD21(-) NK cells produced large amounts of IFN-γ, exhibited highly upregulated expression of mRNAs encoding NK-cell-associated receptors, and demonstrated strong natural killing activity against canine tumor cells. Although the expanded NK cells were dose-dependently cytotoxic to both normal and CDV-infected Vero cells, CDV infection rendered Vero cells more susceptible to NK cells. Pretreatment with anti-CDV serum from hyperimmunized dogs enhanced the antibody-dependent cellular cytotoxicity (ADCC) of NK cells against CDV-infected Vero cells. The culture supernatants of NK cells, added before or after infection, dose-dependently inhibited both CDV replication and development of CDV-induced cytopathic effects (CPEs) in Vero cells. Anti-IFN-γ antibody neutralized the inhibitory effects of NK cell culture supernatants on CDV replication and CPE induction in Vero cells. Such results emphasize the potential significance of NK cells in controlling CDV infection, and indicate that NK cells may play roles both during CDV infection and in combating such infections, under certain conditions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Js] Journal subset:IM
[St] Status:In-Data-Review

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[PMID]: 25769434
[Au] Autor:Oktem O; Guzel Y; Aksoy S; Aydin E; Urman B
[Ad] Address:Associate Professor, Department of Obstetrics and Gynecology, Division Reproductive Endocrinology and Infertility, School of Medicine, Koc University, Istanbul, Turkey....
[Ti] Title:Ovarian function and reproductive outcomes of female patients with systemic lupus erythematosus and the strategies to preserve their fertility.
[So] Source:Obstet Gynecol Surv;70(3):196-210, 2015 Mar.
[Is] ISSN:1533-9866
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Systemic lupus erythematosus (SLE) is a chronic autoimmune systemic disease that mainly affects women of reproductive age. Emerging data from recent molecular studies show us that estrogen hormone plays a central role in the development of this disease. By acting via its cognate receptors ERα and ER expressed on immune cells, estrogen can modulate immune function in both the innate and adaptive immune responses. Interestingly, estrogen may also evoke autoimmune responses after binding to B lymphocytes leading to the generation of high-affinity autoantibodies and proinflammatory cytokines (so-called estrogen-induced autoimmunity). Unfortunately, reproductive function of young female patients with this disease is commonly compromised by different pathophysiologic processes. First, ovarian reserve is diminished even in the presence of mild disease suggesting a direct impact of the disease itself on ovarian function possibly due to ovarian involvement in the form of autoimmune oophoritis. Second, SLE patients with severe manifestations of the disease are treated with alkylating chemotherapy agent cyclophosphamide. Cyclophosphamide and other drugs of alkylating category have the highest gonadotoxicity. Therefore, SLE patients exposed to cyclophosphamide have a much higher risk of developing infertility and premature ovarian failure than do the counterparts who are treated with other less toxic treatments. Third, the functions of the hypothalamic pituitary ovarian axis are perturbed by chronic inflammatory state. And finally adverse pregnancy outcomes are more commonly observed in SLE patients such as fetal loss, preterm birth, intrauterine fetal growth restriction, preeclampsia-eclampsia, and fetal congenital heart block. We aimed in this review article to provide the readers an update on how estrogen hormone closely interacts with and induces lupus-prone changes in the immune system. We also discuss ovarian function and other reproductive outcomes in SLE patients and the current strategies to preserve their fertility in the light of the most recent evidence-based findings of the clinical trials and molecular studies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/OGX.0000000000000160

  3 / 449183 MEDLINE  
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[PMID]: 25361548
[Au] Autor:Zwicker F; Swartman B; Roeder F; Sterzing F; Hauswald H; Thieke C; Weber KJ; Huber PE; Schubert K; Debus J; Herfarth K
[Ad] Address:Department of Radiation Oncology, University of Heidelberg, Im Neuenheimer Feld 400, 69120 Heidelberg, Germany Clinical Cooperation Unit Radiation Oncology, German Cancer Research Center (DKFZ), Heidelberg, Germany f.zwicker@dkfz.de....
[Ti] Title:In vivo measurement of dose distribution in patients' lymphocytes: helical tomotherapy versus step-and-shoot IMRT in prostate cancer.
[So] Source:J Radiat Res;56(2):239-47, 2015 Mar.
[Is] ISSN:1349-9157
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:In radiotherapy, in vivo measurement of dose distribution within patients' lymphocytes can be performed by detecting gamma-H2AX foci in lymphocyte nuclei. This method can help in determining the whole-body dose. Options for risk estimations for toxicities in normal tissue and for the incidence of secondary malignancy are still under debate. In this investigation, helical tomotherapy (TOMO) is compared with step-and-shoot IMRT (SSIMRT) of the prostate gland by measuring the dose distribution within patients' lymphocytes. In this prospective study, blood was taken from 20 patients before and 10 min after their first irradiation fraction for each technique. The isolated leukocytes were fixed 2 h after radiation. DNA double-stranded breaks in lymphocyte nuclei were stained immunocytochemically using anti-gamma-H2AX antibodies. Gamma-H2AX foci distribution in lymphocytes was determined for each patient. Using a calibration line, dose distributions in patients' lymphocytes were determined by studying the gamma-H2AX foci distribution, and these data were used to generate a cumulative dose-lymphocyte histogram (DLH). Measured in vivo (DLH), significantly fewer lymphocytes indicated low-dose exposure (<40% of the applied dose) during TOMO compared with SSIMRT. The dose exposure range, between 45 and 100%, was equal with both radiation techniques. The mean number of gamma-H2AX foci per lymphocyte was significantly lower in the TOMO group compared with the SSIMRT group. In radiotherapy of the prostate gland, TOMO generates a smaller fraction of patients' lymphocytes with low-dose exposure relative to the whole body compared with SSIMRT. Differences in the constructional buildup of the different linear accelerator systems, e.g. the flattening filter, may be the cause thereof. The influence of these methods on the incidence of secondary malignancy should be investigated in further studies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/jrr/rru096

  4 / 449183 MEDLINE  
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[PMID]: 25589622
[Au] Autor:Lee YH; Bae HC; Noh KH; Song KH; Ye SK; Mao CP; Lee KM; Wu TC; Kim TW
[Ad] Address:Division of Infection and Immunology, Graduate School of Medicine, Korea University, Seoul, Korea. Department of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, Korea....
[Ti] Title:Gain of HIF-1α under Normoxia in Cancer Mediates Immune Adaptation through the AKT/ERK and VEGFA Axes.
[So] Source:Clin Cancer Res;21(6):1438-46, 2015 Mar 15.
[Is] ISSN:1078-0432
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: Adaptation to host immune surveillance is now recognized as a hallmark of cancer onset and progression, and represents an early, indispensable event in cancer evolution. This process of evolution is first instigated by an immune selection pressure imposed by natural host surveillance mechanisms and may then be propagated by vaccination or other types of immunotherapy. EXPERIMENTAL DESIGN: We developed a system to simulate cancer evolution in a live host and to dissect the mechanisms responsible for adaptation to immune selection. Here, we show that the oxygen-sensitive α subunit of hypoxia-inducible factor 1 (HIF-1α) plays a central role in cancer immune adaptation under conditions of normal oxygen tension. RESULTS: We found that tumor cells gain HIF-1α in the course of immune selection under normoxia and that HIF-1α renders tumor cells resistant to lysis by tumor-specific cytotoxic T lymphocytes (CTL) in culture and in mice. The effects of HIF-1α on immune adaptation were mediated through VEGFA-dependent activation of the AKT and ERK signaling pathways, which induced an antiapoptotic gene expression network in tumor cells. CONCLUSIONS: Our study therefore establishes a link between immune selection, overexpression of HIF-1α, and cancer immune adaptation under normoxia, providing new opportunities for molecular intervention in patients with cancer. Clin Cancer Res; 21(6); 1438-46. 2015 AACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1158/1078-0432.CCR-14-1979

  5 / 449183 MEDLINE  
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[PMID]: 25691620
[Au] Autor:Case AJ; Zimmerman MC
[Ad] Address:From the Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha (A.J.C., M.C.Z.); and Redox Biology Center, University of Nebraska Lincoln (M.C.Z.).
[Ti] Title:Redox-regulated suppression of splenic T-lymphocyte activation in a model of sympathoexcitation.
[So] Source:Hypertension;65(4):916-23, 2015 Apr.
[Is] ISSN:1524-4563
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Sympathoexcitation, increased circulating norepinephrine, and elevated levels of reactive oxygen species are driving forces underlying numerous cardiovascular diseases, including hypertension. However, the effects of elevated norepinephrine and subsequent reactive oxygen species production in splenic T-lymphocytes during hypertension are not currently understood. We hypothesized that increased systemic levels of norepinephrine inhibits the activation of splenic T-lymphocytes via redox signaling. To address this hypothesis, we examined the status of T-lymphocyte activation in spleens of a mouse model of sympathoexcitation-driven hypertension (ie, norepinephrine infusion). Splenic T-lymphocytes from norepinephrine-infused mice demonstrated decreased proliferation accompanied by a reduction in interferon gamma and tumor necrosis factor-α production as compared with T-lymphocytes from saline-infused mice. Additionally, norepinephrine directly inhibited splenic T-lymphocyte proliferation and cytokine production ex vivo in a dose-dependent manner. Furthermore, norepinephrine caused an increase in G1 arrest in norepinephrine-treated T-lymphocytes, and this was accompanied by a decrease in pro-growth cyclin D3, E1, and E2 mRNA expression. Interestingly, norepinephrine caused an increase in cellular superoxide, which was shown to be partially causal to the inhibitory effects of norepinephrine, as antioxidant supplementation (ie, Tempol) to norepinephrine-infused mice moderately restored T-lymphocyte growth and proinflammatory cytokine production. Our findings indicate that suppression of splenic T-lymphocyte activation occurs in a norepinephrine-driven model of hypertension due to, at least in part, an increase in superoxide. We speculate that further understanding of how norepinephrine mediates its inhibitory effects on splenic T-lymphocytes may elucidate novel pathways for therapeutic mimicry to suppress T-lymphocyte-mediated inflammation in an array of diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150314
[Lr] Last revision date:150314
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1161/HYPERTENSIONAHA.114.05075

  6 / 449183 MEDLINE  
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[PMID]: 25667212
[Au] Autor:Khan NS; Song CY; Jennings BL; Estes AM; Fang XR; Bonventre JV; Malik KU
[Ad] Address:From the Department of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN (N.S.K., C.Y.S., B.L.J., A.M.E., X.R.F., K.U.M.); and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institute of Medicine, Bost...
[Ti] Title:Cytosolic Phospholipase A2α Is Critical for Angiotensin II-Induced Hypertension and Associated Cardiovascular Pathophysiology.
[So] Source:Hypertension;65(4):784-92, 2015 Apr.
[Is] ISSN:1524-4563
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Angiotensin II activates cytosolic phospholipase A(2)α (cPLA2α) and releases arachidonic acid from tissue phospholipids, which mediate or modulate ≥1 cardiovascular effects of angiotensin II and has been implicated in hypertension. Because arachidonic acid release is the rate limiting step in eicosanoid production, cPLA2α might play a central role in the development of angiotensin II-induced hypertension. To test this hypothesis, we investigated the effect of angiotensin II infusion for 13 days by micro-osmotic pumps on systolic blood pressure and associated pathogenesis in wild type (cPLA2α(+/+)) and cPLA2α(-/-) mice. Angiotensin II-induced increase in systolic blood pressure in cPLA2α(+/+) mice was abolished in cPLA2α(-/-) mice; increased systolic blood pressure was also abolished by the arachidonic acid metabolism inhibitor, 5,8,11,14-eicosatetraynoic acid in cPLA2α(+/+) mice. Angiotensin II in cPLA2α(+/+) mice increased cardiac cPLA2 activity and urinary eicosanoid excretion, decreased cardiac output, caused cardiovascular remodeling with endothelial dysfunction, and increased vascular reactivity in cPLA2α(+/+) mice; these changes were diminished in cPLA2α(-/-) mice. Angiotensin II also increased cardiac infiltration of F4/80(+) macrophages and CD3(+) T lymphocytes, cardiovascular oxidative stress, expression of endoplasmic reticulum stress markers p58(IPK), and CHOP in cPLA2α(+/+) but not cPLA2α(-/-) mice. Angiotensin II increased cardiac activity of ERK1/2 and cSrc in cPLA2α(+/+) but not cPLA2α(-/-) mice. These data suggest that angiotensin II-induced hypertension and associated cardiovascular pathophysiological changes are mediated by cPLA2α activation, most likely through the release of arachidonic acid and generation of eicosanoids with predominant prohypertensive effects and activation of ≥1 signaling molecules, including ERK1/2 and cSrc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150314
[Lr] Last revision date:150314
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1161/HYPERTENSIONAHA.114.04803

  7 / 449183 MEDLINE  
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[PMID]: 25667416
[Au] Autor:Boland BS; Widjaja CE; Banno A; Zhang B; Kim SH; Stoven S; Peterson MR; Jones MC; Su HI; Crowe SE; Bui JD; Ho SB; Okugawa Y; Goel A; Marietta EV; Khosroheidari M; Jepsen K; Aramburu J; Lpez-Rodrguez C; Sandborn WJ; Murray JA; Harismendy O; Chang JT
[Ad] Address:Department of Medicine, University of California San Diego, La Jolla, CA 92093; Inflammatory Bowel Disease Center, University of California San Diego, La Jolla, CA 92093;...
[Ti] Title:Immunodeficiency and autoimmune enterocolopathy linked to NFAT5 haploinsufficiency.
[So] Source:J Immunol;194(6):2551-60, 2015 Mar 15.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The link between autoimmune diseases and primary immunodeficiency syndromes has been increasingly appreciated. Immunologic evaluation of a young man with autoimmune enterocolopathy and unexplained infections revealed evidence of immunodeficiency, including IgG subclass deficiency, impaired Ag-induced lymphocyte proliferation, reduced cytokine production by CD8(+) T lymphocytes, and decreased numbers of NK cells. Genetic evaluation identified haploinsufficiency of NFAT5, a transcription factor regulating immune cell function and cellular adaptation to hyperosmotic stress, as a possible cause of this syndrome. Inhibition or deletion of NFAT5 in normal human and murine cells recapitulated several of the immune deficits identified in the patient. These results provide evidence of a primary immunodeficiency disorder associated with organ-specific autoimmunity linked to NFAT5 deficiency.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150314
[Lr] Last revision date:150314
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1401463

  8 / 449183 MEDLINE  
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[PMID]: 25454632
[Au] Autor:Cassady JP; D'Alessio AC; Sarkar S; Dani VS; Fan ZP; Ganz K; Roessler R; Sur M; Young RA; Jaenisch R
[Ad] Address:The Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA....
[Ti] Title:Direct lineage conversion of adult mouse liver cells and B lymphocytes to neural stem cells.
[So] Source:Stem Cell Reports;3(6):948-56, 2014 Dec 9.
[Is] ISSN:2213-6711
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Overexpression of transcription factors has been used to directly reprogram somatic cells into a range of other differentiated cell types, including multipotent neural stem cells (NSCs), that can be used to generate neurons and glia. However, the ability to maintain the NSC state independent of the inducing factors and the identity of the somatic donor cells remain two important unresolved issues in transdifferentiation. Here we used transduction of doxycycline-inducible transcription factors to generate stable tripotent NSCs. The induced NSCs (iNSCs) maintained their characteristics in the absence of exogenous factor expression and were transcriptionally, epigenetically, and functionally similar to primary brain-derived NSCs. Importantly, we also generated tripotent iNSCs from multiple adult cell types, including mature liver and B cells. Our results show that self-maintaining proliferative neural cells can be induced from nonectodermal cells by expressing specific combinations of transcription factors.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1412
[Cu] Class update date: 150314
[Lr] Last revision date:150314
[Js] Journal subset:IM
[St] Status:In-Process

  9 / 449183 MEDLINE  
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[PMID]: 25378593
[Au] Autor:Mikacenic C; Schneider A; Radella F; Buckner JH; Wurfel MM
[Ad] Address:Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, WA 98104; and cmikacen@uw.edu....
[Ti] Title:Cutting edge: Genetic variation in TLR1 is associated with Pam3CSK4-induced effector T cell resistance to regulatory T cell suppression.
[So] Source:J Immunol;193(12):5786-90, 2014 Dec 15.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:TLR play essential roles in the initiation and modulation of immune responses. TLR1/TLR2 heterodimers recognize triacylated bacterial lipopeptides, including the synthetic TLR1/2 lipopeptide Pam3CSK4. Genetic variation in TLR1 is associated with outcomes in diseases in which regulatory T cells (Treg) play a role, including asthma and allergy. To determine whether genetic polymorphisms in TLR1 are associated with alterations in Treg suppression of effector T cells (Teff), we performed in vitro suppression assays in healthy individuals with various haplotypes in TLR1. We show that functional genetic polymorphisms in TLR1 modify surface expression of TLR1 on T lymphocytes and confer enhanced Teff resistance to Treg suppression in the presence of Pam3CSK4. These effects are mediated, in part, by IL-6 and inhibited by blocking IL-6 signaling through STAT3. These findings suggest that TLR1 polymorphisms could influence immune-related disease through Teff resistance to Treg suppression.
[Mh] MeSH terms primary: Genetic Variation
T-Lymphocyte Subsets/immunology
T-Lymphocyte Subsets/metabolism
T-Lymphocytes, Regulatory/immunology
Toll-Like Receptor 1/genetics
Toll-Like Receptor 1/metabolism
[Mh] MeSH terms secundary: Alleles
Cell Membrane/metabolism
Haplotypes
Humans
Immunomodulation/genetics
Interleukin-6/biosynthesis
Lipopeptides/pharmacology
Polymorphism, Single Nucleotide
STAT3 Transcription Factor/antagonists & inhibitors
T-Lymphocyte Subsets/drug effects
T-Lymphocytes, Regulatory/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Interleukin-6); 0 (Lipopeptides); 0 (Pam(3)CSK(4) peptide); 0 (STAT3 Transcription Factor); 0 (Toll-Like Receptor 1)
[Em] Entry month:1503
[Cu] Class update date: 150314
[Lr] Last revision date:150314
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:141206
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1401185

  10 / 449183 MEDLINE  
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[PMID]: 25304264
[Au] Autor:Sahu RP; Ocana JA; Harrison KA; Ferracini M; Touloukian CE; Al-Hassani M; Sun L; Loesch M; Murphy RC; Althouse SK; Perkins SM; Speicher PJ; Tyler DS; Konger RL; Travers JB
[Ad] Address:Department of Dermatology, Indiana University School of Medicine, Indianapolis, Indiana. Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana....
[Ti] Title:Chemotherapeutic agents subvert tumor immunity by generating agonists of platelet-activating factor.
[So] Source:Cancer Res;74(23):7069-78, 2014 Dec 1.
[Is] ISSN:1538-7445
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Oxidative stress suppresses host immunity by generating oxidized lipid agonists of the platelet-activating factor receptor (PAF-R). Because many classical chemotherapeutic drugs induce reactive oxygen species (ROS), we investigated whether these drugs might subvert host immunity by activating PAF-R. Here, we show that PAF-R agonists are produced in melanoma cells by chemotherapy that is administered in vitro, in vivo, or in human subjects. Structural characterization of the PAF-R agonists induced revealed multiple oxidized glycerophosphocholines that are generated nonenzymatically. In a murine model of melanoma, chemotherapeutic administration could augment tumor growth by a PAF-R-dependent process that could be blocked by treatment with antioxidants or COX-2 inhibitors or by depletion of regulatory T cells. Our findings reveal how PAF-R agonists induced by chemotherapy treatment can promote treatment failure. Furthermore, they offer new insights into how to improve the efficacy of chemotherapy by blocking its heretofore unknown impact on PAF-R activation.
[Mh] MeSH terms primary: Antineoplastic Agents/immunology
Antineoplastic Agents/pharmacology
Melanoma, Experimental/drug therapy
Melanoma, Experimental/immunology
Platelet Activating Factor/agonists
[Mh] MeSH terms secundary: Animals
Antioxidants/pharmacology
Cell Line, Tumor
Cyclooxygenase 2 Inhibitors/immunology
Cyclooxygenase 2 Inhibitors/pharmacology
Female
Glycerylphosphorylcholine/immunology
Glycerylphosphorylcholine/metabolism
Humans
Mice
Mice, Inbred C57BL
Oxidative Stress/drug effects
Oxidative Stress/immunology
Platelet Activating Factor/immunology
Platelet Activating Factor/metabolism
Platelet Membrane Glycoproteins/immunology
Platelet Membrane Glycoproteins/metabolism
Reactive Oxygen Species/immunology
Reactive Oxygen Species/metabolism
Receptors, G-Protein-Coupled/immunology
Receptors, G-Protein-Coupled/metabolism
Signal Transduction/drug effects
Signal Transduction/immunology
T-Lymphocytes, Regulatory/drug effects
T-Lymphocytes, Regulatory/immunology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Antioxidants); 0 (Cyclooxygenase 2 Inhibitors); 0 (Platelet Activating Factor); 0 (Platelet Membrane Glycoproteins); 0 (Reactive Oxygen Species); 0 (Receptors, G-Protein-Coupled); 0 (platelet activating factor receptor); 60M22SGW66 (Glycerylphosphorylcholine)
[Em] Entry month:1503
[Cu] Class update date: 150314
[Lr] Last revision date:150314
[Js] Journal subset:IM
[Da] Date of entry for processing:141202
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-14-2043


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