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  • 1
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    Anomalous type 17 response to viral infection by CD8+ T cells lacking T-bet and eomesodermin (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-19
    Description: When intracellular pathogens invade mammalian hosts, naive CD8+ T cells differentiate into cytotoxic killers, which lyse infected target cells and secrete cytokines that activate intracellular microbicides. We show that CD8+ T cells deficient in the transcription factors T-bet and eomesodermin (Eomes) fail to differentiate into functional killers required for defense against lymphocytic choriomeningitis virus. Instead, virus-specific CD8+ T cells lacking both T-bet and Eomes differentiate into an interleukin-17-secreting lineage, reminiscent of the helper T cell fate that has been implicated in autoimmunity and extracellular microbial defense. Upon viral infection, mice with T cells lacking both T-bet and Eomes develop a CD8+ T cell-dependent, progressive inflammatory and wasting syndrome characterized by multi-organ infiltration of neutrophils. T-bet and Eomes, thus, ensure that CD8+ T cells adopt an appropriate course of intracellular rather than extracellular destruction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807624/" 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/PMC2807624/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Intlekofer, Andrew M -- Banerjee, Arnob -- Takemoto, Naofumi -- Gordon, Scott M -- Dejong, Caitlin S -- Shin, Haina -- Hunter, Christopher A -- Wherry, E John -- Lindsten, Tullia -- Reiner, Steven L -- AI007532/AI/NIAID NIH HHS/ -- AI042334/AI/NIAID NIH HHS/ -- AI042370/AI/NIAID NIH HHS/ -- AI061699/AI/NIAID NIH HHS/ -- AI071309/AI/NIAID NIH HHS/ -- AI076458/AI/NIAID NIH HHS/ -- R01 AI042370/AI/NIAID NIH HHS/ -- R01 AI042370-12/AI/NIAID NIH HHS/ -- R01 AI061699/AI/NIAID NIH HHS/ -- R01 AI061699-05/AI/NIAID NIH HHS/ -- R01 AI071309/AI/NIAID NIH HHS/ -- R01 AI071309-01/AI/NIAID NIH HHS/ -- R01 AI076458/AI/NIAID NIH HHS/ -- R01 AI076458-02/AI/NIAID NIH HHS/ -- T32 CA009140/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Jul 18;321(5887):408-11. doi: 10.1126/science.1159806.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18635804" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Viral/immunology ; Arenaviridae Infections/*immunology/pathology/virology ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/*immunology/*metabolism ; Cell Differentiation ; Cytotoxicity, Immunologic ; Interferon-gamma/metabolism ; Interleukin-17/*metabolism ; Lymphocyte Depletion ; *Lymphocytic choriomeningitis virus/immunology/isolation & ; purification/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; T-Box Domain Proteins/deficiency/genetics/*physiology ; Virus Replication ; Wasting Syndrome/immunology/pathology/virology
    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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  • 2
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    Progenitor and terminal subsets of CD8+ T cells cooperate to contain chronic viral infection (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-01
    Description: Chronic infections strain the regenerative capacity of antiviral T lymphocyte populations, leading to failure in long-term immunity. The cellular and molecular events controlling this regenerative capacity, however, are unknown. We found that two distinct states of virus-specific CD8(+) T cells exist in chronically infected mice and humans. Differential expression of the T-box transcription factors T-bet and Eomesodermin (Eomes) facilitated the cooperative maintenance of the pool of antiviral CD8(+) T cells during chronic viral infection. T-bet(hi) cells displayed low intrinsic turnover but proliferated in response to persisting antigen, giving rise to Eomes(hi) terminal progeny. Genetic elimination of either subset resulted in failure to control chronic infection, which suggests that an imbalance in differentiation and renewal could underlie the collapse of immunity in humans with chronic infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653769/" 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/PMC3653769/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paley, Michael A -- Kroy, Daniela C -- Odorizzi, Pamela M -- Johnnidis, Jonathan B -- Dolfi, Douglas V -- Barnett, Burton E -- Bikoff, Elizabeth K -- Robertson, Elizabeth J -- Lauer, Georg M -- Reiner, Steven L -- Wherry, E John -- 059312/Wellcome Trust/United Kingdom -- AI061699/AI/NIAID NIH HHS/ -- AI0663445/AI/NIAID NIH HHS/ -- AI076458/AI/NIAID NIH HHS/ -- AI078897/AI/NIAID NIH HHS/ -- AI082630/AI/NIAID NIH HHS/ -- AI083022/AI/NIAID NIH HHS/ -- HHSN266200500030C/AI/NIAID NIH HHS/ -- HHSN266200500030C/PHS HHS/ -- P01 AI078897/AI/NIAID NIH HHS/ -- P30 CA016520/CA/NCI NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 AI042370/AI/NIAID NIH HHS/ -- R01 AI061699/AI/NIAID NIH HHS/ -- R01 AI076458/AI/NIAID NIH HHS/ -- T32 AI007632/AI/NIAID NIH HHS/ -- T32-AI-07324/AI/NIAID NIH HHS/ -- U19 AI082630/AI/NIAID NIH HHS/ -- U19 AI083022/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 30;338(6111):1220-5. doi: 10.1126/science.1229620.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23197535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology ; Hepatitis B, Chronic/*immunology ; Humans ; Liver/virology ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Stem Cells/immunology ; T-Box Domain Proteins/genetics/*metabolism ; T-Lymphocyte Subsets/*immunology
    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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  • 3
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    Immunology. An interferon paradox (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Odorizzi, Pamela M -- Wherry, E John -- T32 AI007632/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Apr 12;340(6129):155-6. doi: 10.1126/science.1237568.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Immunology and Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23580520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arenaviridae Infections/*immunology/*virology ; Female ; Interferon Type I/*immunology/*metabolism ; Lymphocytic choriomeningitis virus/*immunology/*physiology ; Male ; *Signal Transduction
    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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  • 4
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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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  • 5
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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
    Published by American Association for the Advancement of Science (AAAS)
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