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  • 1
    Publication Date: 2012-10-30
    Description: The mammalian host has developed a long-standing symbiotic relationship with a considerable number of microbial species. These include the microbiota on environmental surfaces, such as the respiratory and gastrointestinal tracts, and also endogenous retroviruses (ERVs), comprising a substantial fraction of the mammalian genome. The long-term consequences for the host of interactions with these microbial species can range from mutualism to parasitism and are not always completely understood. The potential effect of one microbial symbiont on another is even less clear. Here we study the control of ERVs in the commonly used C57BL/6 (B6) mouse strain, which lacks endogenous murine leukaemia viruses (MLVs) able to replicate in murine cells. We demonstrate the spontaneous emergence of fully infectious ecotropic MLV in B6 mice with a range of distinct immune deficiencies affecting antibody production. These recombinant retroviruses establish infection of immunodeficient mouse colonies, and ultimately result in retrovirus-induced lymphomas. Notably, ERV activation in immunodeficient mice is prevented in husbandry conditions associated with reduced or absent intestinal microbiota. Our results shed light onto a previously unappreciated role for immunity in the control of ERVs and provide a potential mechanistic link between immune activation by microbial triggers and a range of pathologies associated with ERVs, including cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511586/" 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/PMC3511586/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, George R -- Eksmond, Urszula -- Salcedo, Rosalba -- Alexopoulou, Lena -- Stoye, Jonathan P -- Kassiotis, George -- MC_U117512710/Medical Research Council/United Kingdom -- MC_U117581330/Medical Research Council/United Kingdom -- U.1175.02.005.00005(60891)/Medical Research Council/United Kingdom -- U.1175.02.006.00007(81330)/Medical Research Council/United Kingdom -- U117512710/Medical Research Council/United Kingdom -- U117581330/Medical Research Council/United Kingdom -- England -- Nature. 2012 Nov 29;491(7426):774-8. doi: 10.1038/nature11599. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunoregulation, MRC National Institute for Medical Research, The Ridgeway, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103862" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry ; Animals ; Antibodies, Viral/*biosynthesis/immunology ; Cell Transformation, Viral ; Endogenous Retroviruses/genetics/growth & development/immunology/*physiology ; Female ; Immunocompromised Host/*immunology ; Leukemia/virology ; Leukemia Virus, Murine/genetics/growth & development/immunology/physiology ; Lymphoma/virology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/deficiency/genetics ; Recombination, Genetic ; Viremia/immunology/virology ; *Virus Activation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2006-06-03
    Description: Dominant mutations in superoxide dismutase cause amyotrophic lateral sclerosis (ALS), a progressive paralytic disease characterized by loss of motor neurons. With the use of mice carrying a deletable mutant gene, expression within motor neurons was shown to be a primary determinant of disease onset and of an early phase of disease progression. Diminishing the mutant levels in microglia had little effect on the early disease phase but sharply slowed later disease progression. Onset and progression thus represent distinct disease phases defined by mutant action within different cell types to generate non-cell-autonomous killing of motor neurons; these findings validate therapies, including cell replacement, targeted to the non-neuronal cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boillee, Severine -- Yamanaka, Koji -- Lobsiger, Christian S -- Copeland, Neal G -- Jenkins, Nancy A -- Kassiotis, George -- Kollias, George -- Cleveland, Don W -- MC_U117581330/Medical Research Council/United Kingdom -- NS 27036/NS/NINDS NIH HHS/ -- R37 NS027036/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 2;312(5778):1389-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research and Departments of Medicine and Neuroscience, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16741123" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*enzymology/genetics/pathology/physiopathology ; Animals ; Antigens, CD11b/genetics ; Disease Progression ; Female ; Humans ; Integrases/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/*metabolism ; Motor Neurons/*metabolism ; Mutation ; Superoxide Dismutase/genetics/*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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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2008-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kassiotis, George -- O'Garra, Anne -- MC_U117565642/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 May 30;320(5880):1168-9. doi: 10.1126/science.1159090.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunoregulation, MRC National Institute for Medical Research, The Ridgeway, London NW7 1AA, UK. gkassio@nimr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18511677" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Herpes Genitalis/*immunology ; Humans ; Immune Tolerance ; Lymph Nodes/immunology ; T-Lymphocytes, Regulatory/*immunology ; Vaginal Diseases/*immunology/virology
    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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