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  • Mice, Inbred C57BL  (39)
  • American Association for the Advancement of Science (AAAS)  (39)
  • Elsevier
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  • 1
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    Coinfection. Virus-helminth coinfection reveals a microbiota-independent mechanism of immunomodulation (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-08-02
    Description: The mammalian intestine is colonized by beneficial commensal bacteria and is a site of infection by pathogens, including helminth parasites. Helminths induce potent immunomodulatory effects, but whether these effects are mediated by direct regulation of host immunity or indirectly through eliciting changes in the microbiota is unknown. We tested this in the context of virus-helminth coinfection. Helminth coinfection resulted in impaired antiviral immunity and was associated with changes in the microbiota and STAT6-dependent helminth-induced alternative activation of macrophages. Notably, helminth-induced impairment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-like molecule that is associated with alternatively activated macrophages, could partially restore antiviral immunity. These data indicate that helminth-induced immunomodulation occurs independently of changes in the microbiota but is dependent on Ym1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548887/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548887/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osborne, Lisa C -- Monticelli, Laurel A -- Nice, Timothy J -- Sutherland, Tara E -- Siracusa, Mark C -- Hepworth, Matthew R -- Tomov, Vesselin T -- Kobuley, Dmytro -- Tran, Sara V -- Bittinger, Kyle -- Bailey, Aubrey G -- Laughlin, Alice L -- Boucher, Jean-Luc -- Wherry, E John -- Bushman, Frederic D -- Allen, Judith E -- Virgin, Herbert W -- Artis, David -- 095831/Wellcome Trust/United Kingdom -- 2-P30 CA016520/CA/NCI NIH HHS/ -- 5T32A100716334/PHS HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI082630/AI/NIAID NIH HHS/ -- AI083022/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI097333/AI/NIAID NIH HHS/ -- AI102942/AI/NIAID NIH HHS/ -- AI106697/AI/NIAID NIH HHS/ -- F32 AI085828/AI/NIAID NIH HHS/ -- F32-AI085828/AI/NIAID NIH HHS/ -- HHSN272201300006C/PHS HHS/ -- K08 DK097301/DK/NIDDK NIH HHS/ -- K08-DK097301/DK/NIDDK NIH HHS/ -- MR/J001929/1/Medical Research Council/United Kingdom -- P01 AI106697/AI/NIAID NIH HHS/ -- P30-AI045008/AI/NIAID NIH HHS/ -- P30-DK050306/DK/NIDDK NIH HHS/ -- R01 AI 084887/AI/NIAID NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI097333/AI/NIAID NIH HHS/ -- R01 AI102942/AI/NIAID NIH HHS/ -- R21 AI087990/AI/NIAID NIH HHS/ -- T32-AI007532/AI/NIAID NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 1;345(6196):578-82. doi: 10.1126/science.1256942. Epub 2014 Jul 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques, Universite Paris Descartes, Paris, France. ; Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. dartis@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25082704" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/immunology ; Caliciviridae Infections/*immunology ; Coinfection/*immunology/microbiology/parasitology ; Gastroenteritis/*immunology/virology ; Germ-Free Life ; *Immunomodulation ; Intestines/immunology/microbiology/virology ; Lectins/*immunology ; Macrophage Activation ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Microbiota/*immunology ; Norovirus/*immunology ; Trichinella/*immunology ; Trichinellosis/*immunology ; beta-N-Acetylhexosaminidases/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Vaccine-elicited CD4 T cells induce immunopathology after chronic LCMV infection (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-01-17
    Description: CD4 T cells promote innate and adaptive immune responses, but how vaccine-elicited CD4 T cells contribute to immune protection remains unclear. We evaluated whether induction of virus-specific CD4 T cells by vaccination would protect mice against infection with chronic lymphocytic choriomeningitis virus (LCMV). Immunization with vaccines that selectively induced CD4 T cell responses resulted in catastrophic inflammation and mortality after challenge with a persistent strain of LCMV. Immunopathology required antigen-specific CD4 T cells and was associated with a cytokine storm, generalized inflammation, and multi-organ system failure. Virus-specific CD8 T cells or antibodies abrogated the pathology. These data demonstrate that vaccine-elicited CD4 T cells in the absence of effective antiviral immune responses can trigger lethal immunopathology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4382081/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4382081/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Penaloza-MacMaster, Pablo -- Barber, Daniel L -- Wherry, E John -- Provine, Nicholas M -- Teigler, Jeffrey E -- Parenteau, Lily -- Blackmore, Stephen -- Borducchi, Erica N -- Larocca, Rafael A -- Yates, Kathleen B -- Shen, Hao -- Haining, W Nicholas -- Sommerstein, Rami -- Pinschewer, Daniel D -- Ahmed, Rafi -- Barouch, Dan H -- AI007245/AI/NIAID NIH HHS/ -- AI030048/AI/NIAID NIH HHS/ -- AI07387/AI/NIAID NIH HHS/ -- AI078526/AI/NIAID NIH HHS/ -- AI096040/AI/NIAID NIH HHS/ -- P51 OD011132/OD/NIH HHS/ -- T32 AI007245/AI/NIAID NIH HHS/ -- U19 AI078526/AI/NIAID NIH HHS/ -- U19 AI096040/AI/NIAID NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 16;347(6219):278-82. doi: 10.1126/science.aaa2148.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. ; Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. ; Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. ; Department of Pathology and Immunology, WHO Collaborating Centre for Vaccine Immunology, University of Geneva, 1211 Geneva, Switzerland. ; Department of Pathology and Immunology, WHO Collaborating Centre for Vaccine Immunology, University of Geneva, 1211 Geneva, Switzerland. Department of Biomedicine-Haus Petersplatz, Division of Experimental Virology, University of Basel, 4009 Basel, Switzerland. ; Emory Vaccine Center and Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA. ; Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. Ragon Institute of MGH, MIT, and Harvard, Boston, MA 02114, USA. dbarouch@bidmc.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25593185" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Antibodies, Viral/immunology ; Antigens, Viral/immunology ; Arenaviridae Infections/*immunology/virology ; CD4-Positive T-Lymphocytes/*immunology ; CD8-Positive T-Lymphocytes/immunology ; Cytokines/blood ; Epitopes, T-Lymphocyte/immunology ; Immune System Diseases/*etiology/immunology/pathology ; Immunologic Memory ; Inflammation/*etiology/immunology/pathology ; Lymphocytic choriomeningitis virus/*immunology/physiology ; Mice, Inbred C57BL ; Multiple Organ Failure/etiology ; Vaccination ; Viral Load ; Viral Vaccines/*adverse effects/*immunology ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Transgenic mouse model of stunned myocardium (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-22
    Description: Stunned myocardium is a syndrome of reversible contractile failure that frequently complicates coronary artery disease. Cardiac excitation is uncoupled from contraction at the level of the myofilaments. Selective proteolysis of the thin filament protein troponin I has been correlated with stunned myocardium. Here, transgenic mice expressing the major degradation product of troponin I (TnI1-193) in the heart were found to develop ventricular dilatation, diminished contractility, and reduced myofilament calcium responsiveness, recapitulating the phenotype of stunned myocardium. Proteolysis of troponin I also occurs in ischemic human cardiac muscle. Thus, troponin I proteolysis underlies the pathogenesis of a common acquired form of heart failure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, A M -- Kogler, H -- Georgakopoulos, D -- McDonough, J L -- Kass, D A -- Van Eyk, J E -- Marban, E -- HL 44065/HL/NHLBI NIH HHS/ -- HL 63038/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):488-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Johns Hopkins University School of Medicine, Ross Building 1144, 720 Rutland Avenue, Baltimore, MD 21205, USA. murphy@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642551" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism ; Adrenergic beta-Agonists/pharmacology ; Animals ; Calcium/metabolism ; Cardiomegaly/pathology ; Dilatation, Pathologic ; *Disease Models, Animal ; Heart Rate ; Heart Ventricles/pathology ; Humans ; Isoproterenol/pharmacology ; Mice ; Mice, Inbred C57BL ; *Mice, Transgenic ; Myocardial Contraction ; Myocardial Stunning/*metabolism/pathology/physiopathology ; Myocardium/*metabolism/pathology ; Myofibrils/metabolism ; Troponin I/genetics/*metabolism ; Ventricular Function, Left
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Enhanced tumor formation in mice heterozygous for Blm mutation (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-21
    Description: Persons with the autosomal recessive disorder Bloom syndrome are predisposed to cancers of many types due to loss-of-function mutations in the BLM gene, which encodes a recQ-like helicase. Here we show that mice heterozygous for a targeted null mutation of Blm, the murine homolog of BLM, develop lymphoma earlier than wild-type littermates in response to challenge with murine leukemia virus and develop twice the number of intestinal tumors when crossed with mice carrying a mutation in the Apc tumor suppressor. These observations indicate that Blm is a modifier of tumor formation in the mouse and that Blm haploinsufficiency is associated with tumor predisposition, a finding with important implications for cancer risk in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goss, Kathleen Heppner -- Risinger, Mary A -- Kordich, Jennifer J -- Sanz, Maureen M -- Straughen, Joel E -- Slovek, Lisa E -- Capobianco, Anthony J -- German, James -- Boivin, Gregory P -- Groden, Joanna -- CA63507/CA/NCI NIH HHS/ -- CA84291/CA/NCI NIH HHS/ -- CA88460/CA/NCI NIH HHS/ -- ES06096/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2002 Sep 20;297(5589):2051-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Department of Molecular Genetics, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12242442" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/pathology ; Adenosine Triphosphatases/*genetics ; Alleles ; Animals ; Bloom Syndrome/*genetics ; Cells, Cultured ; Crosses, Genetic ; DNA Helicases/*genetics ; Female ; Gene Targeting ; Genes, APC ; *Genetic Predisposition to Disease ; *Heterozygote ; Humans ; Intestinal Neoplasms/*genetics/pathology ; Leukemia Virus, Murine ; Loss of Heterozygosity ; Lymphoma, T-Cell/*genetics/virology ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; RecQ Helicases ; Sister Chromatid Exchange
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Fertilization defects in sperm from mice lacking fertilin beta (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-22
    Description: Fertilin, a member of the ADAM family, is found on the plasma membrane of mammalian sperm. Sperm from mice lacking fertilin beta were shown to be deficient in sperm-egg membrane adhesion, sperm-egg fusion, migration from the uterus into the oviduct, and binding to the egg zona pellucida. Egg activation was unaffected. The results are consistent with a direct role of fertilin in sperm-egg plasma membrane interaction. Fertilin could also have a direct role in sperm-zona binding or oviduct migration; alternatively, the effects on these functions could result from the absence of fertilin activity during spermatogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, C -- Bunch, D O -- Faure, J E -- Goulding, E H -- Eddy, E M -- Primakoff, P -- Myles, D G -- HD16580/HD/NICHD NIH HHS/ -- U54HD29125/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 18;281(5384):1857-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular and Cellular Biology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9743500" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Animals ; Calcium/metabolism ; Cell Adhesion ; Cell Membrane/physiology ; Fallopian Tubes ; Female ; Male ; Membrane Fusion ; Membrane Glycoproteins/genetics/metabolism/*physiology ; Metalloendopeptidases/genetics/metabolism/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Ovum/physiology ; Sperm Capacitation ; *Sperm-Ovum Interactions ; Spermatogenesis ; Spermatozoa/chemistry/*physiology ; Zona Pellucida/physiology
    Print ISSN: 0036-8075
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  • 7
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    Delivery of epitopes by the Salmonella type III secretion system for vaccine development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-24
    Description: Avirulent strains of Salmonella typhimurium are being considered as antigen delivery vectors. During its intracellular stage in the host, S. typhimurium resides within a membrane-bound compartment and is not an efficient inducer of class I-restricted immune responses. Viral epitopes were successfully delivered to the host-cell cytosol by using the type III protein secretion system of S. typhimurium. This resulted in class I-restricted immune responses that protected vaccinated animals against lethal infection. This approach may allow the efficient use of S. typhimurium as an antigen delivery system to control infections by pathogens that require this type of immune response for protection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russmann, H -- Shams, H -- Poblete, F -- Fu, Y -- Galan, J E -- Donis, R O -- New York, N.Y. -- Science. 1998 Jul 24;281(5376):565-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, School of Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794-5222, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9677200" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigens, Viral/immunology/metabolism ; Bacterial Proteins/genetics/*metabolism ; Cytosol/*immunology ; Endoplasmic Reticulum/immunology/metabolism ; Epitopes/*immunology ; Histocompatibility Antigens Class I/immunology ; Hybridomas ; Lymphocytic Choriomeningitis/prevention & control ; Lymphocytic choriomeningitis virus/immunology ; Mice ; Mice, Inbred C57BL ; Nucleoproteins/immunology/metabolism ; Peptide Fragments/immunology/metabolism ; Protein Tyrosine Phosphatases/genetics/*metabolism ; Recombinant Fusion Proteins/immunology/metabolism ; *Salmonella typhimurium/metabolism/pathogenicity ; T-Lymphocytes/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Tumor Cells, Cultured ; Vaccines, Synthetic/*administration & dosage/immunology ; Viral Core Proteins/immunology/metabolism ; Viral Vaccines/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Regulation of alloreactivity in vivo by a soluble form of the interleukin-1 receptor (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: In vitro studies have shown that cytokines are involved in the regulation of the immune response, but their role in vivo is less well defined. Specific cytokine antagonists enable the identification of particular cytokines involved in the response and offer a means for modifying it. Systemic administration of a soluble, extracellular portion of the receptor for interleukin-1 (sIL-1R) had profound inhibitory effects on the development of in vivo alloreactivity. Survival of heterotopic heart allografts was prolonged from 12 days in controls to 17 days in mice treated with sIL-1R. Lymph node hyperplasia in response to a localized injection of allogeneic cells was completely blocked by sIL-1R treatment. The inhibition was overcome by simultaneous administration of interleukin-1 (IL-1); thus, sIL-1R acts by neutralizing IL-1. These results implicate IL-1 as a regulator of allograft rejection and demonstrate the in vivo biological efficacy of a soluble cytokine receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fanslow, W C -- Sims, J E -- Sassenfeld, H -- Morrissey, P J -- Gillis, S -- Dower, S K -- Widmer, M B -- New York, N.Y. -- Science. 1990 May 11;248(4956):739-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2139736" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Graft Rejection ; *Graft Survival ; H-2 Antigens/immunology ; Heart Transplantation/*immunology ; Immunosuppression ; Interleukin-1/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/immunology ; Receptors, Immunologic/*immunology ; Receptors, Interleukin-1 ; Transplantation, Heterotopic ; Transplantation, Homologous
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  • 9
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    Neurokinin 1 receptor antagonism as a possible therapy for alcoholism (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-16
    Description: Alcohol dependence is a major public health challenge in need of new treatments. As alcoholism evolves, stress systems in the brain play an increasing role in motivating continued alcohol use and relapse. We investigated the role of the neurokinin 1 receptor (NK1R), a mediator of behavioral stress responses, in alcohol dependence and treatment. In preclinical studies, mice genetically deficient in NK1R showed a marked decrease in voluntary alcohol consumption and had an increased sensitivity to the sedative effects of alcohol. In a randomized controlled experimental study, we treated recently detoxified alcoholic inpatients with an NK1R antagonist (LY686017; n = 25) or placebo (n = 25). LY686017 suppressed spontaneous alcohol cravings, improved overall well-being, blunted cravings induced by a challenge procedure, and attenuated concomitant cortisol responses. Brain functional magnetic resonance imaging responses to affective stimuli likewise suggested beneficial LY686017 effects. Thus, as assessed by these surrogate markers of efficacy, NK1R antagonism warrants further investigation as a treatment in alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉George, David T -- Gilman, Jodi -- Hersh, Jacqueline -- Thorsell, Annika -- Herion, David -- Geyer, Christopher -- Peng, Xiaomei -- Kielbasa, William -- Rawlings, Robert -- Brandt, John E -- Gehlert, Donald R -- Tauscher, Johannes T -- Hunt, Stephen P -- Hommer, Daniel -- Heilig, Markus -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 14;319(5869):1536-9. doi: 10.1126/science.1153813. Epub 2008 Feb 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276852" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; *Alcohol Drinking/drug therapy ; Alcoholism/*drug therapy ; Animals ; Behavior, Addictive/drug therapy ; Brain/drug effects/physiology ; Emotions/drug effects ; Ethanol/administration & dosage/pharmacology ; Female ; Humans ; Hydrocortisone/blood ; Magnetic Resonance Imaging ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; *Neurokinin-1 Receptor Antagonists ; Pyridines/administration & dosage/pharmacology/*therapeutic use ; Receptors, Neurokinin-1/deficiency/genetics/*physiology ; Triazoles/administration & dosage/pharmacology/*therapeutic use
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Platelets kill intraerythrocytic malarial parasites and mediate survival to infection (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-07
    Description: Platelets play a critical role in the pathogenesis of malarial infections by encouraging the sequestration of infected red blood cells within the cerebral vasculature. But platelets also have well-established roles in innate protection against microbial infections. We found that purified human platelets killed Plasmodium falciparum parasites cultured in red blood cells. Inhibition of platelet function by aspirin and other platelet inhibitors abrogated the lethal effect human platelets exert on P. falciparum parasites. Likewise, platelet-deficient and aspirin-treated mice were more susceptible to death during erythrocytic infection with Plasmodium chabaudi. Both mouse and human platelets bind malarial-infected red cells and kill the parasite within. These results indicate a protective function for platelets in the early stages of erythrocytic infection distinct from their role in cerebral malaria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMorran, Brendan J -- Marshall, Vikki M -- de Graaf, Carolyn -- Drysdale, Karen E -- Shabbar, Meriam -- Smyth, Gordon K -- Corbin, Jason E -- Alexander, Warren S -- Foote, Simon J -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Feb 6;323(5915):797-800. doi: 10.1126/science.1166296.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Menzies Research Institute, University of Tasmania, Private Bag 23, Hobart, Tasmania 7000, Australia. brendan.mcmorran@utas.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19197068" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate/metabolism ; Animals ; Aspirin/pharmacology ; Blood Platelets/metabolism/*physiology ; Erythrocytes/*parasitology ; Female ; Humans ; In Situ Nick-End Labeling ; Malaria/*blood/immunology/*parasitology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Plasmodium chabaudi/*growth & development ; Plasmodium falciparum/*growth & development ; Platelet Activation ; Platelet Aggregation Inhibitors/pharmacology ; Platelet Count ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2Y1 ; Receptors, Thrombopoietin/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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