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    IL-21R on T cells is critical for sustained functionality and control of chronic viral infection (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: Chronic viral infection is often associated with the dysfunction of virus-specific T cells. Our studies using Il21r-deficient (Il21r-/-) mice now suggest that interleukin-21 (IL-21) is critical for the long-term maintenance and functionality of CD8+ T cells and the control of chronic lymphocytic choriomeningitis virus infection in mice. Cell-autonomous IL-21 receptor (IL-21R)-dependent signaling by CD8+ T cells was required for sustained cell proliferation and cytokine production during chronic infection. Il21r-/- mice showed normal CD8+ T cell expansion, effector function, memory homeostasis, and recall responses during acute and after resolved infection with several other nonpersistent viruses. These data suggest that IL-21R signaling is required for the maintenance of polyfunctional T cells during chronic viral infections and have implications for understanding the immune response to other persisting antigens, such as tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frohlich, Anja -- Kisielow, Jan -- Schmitz, Iwana -- Freigang, Stefan -- Shamshiev, Abdijapar T -- Weber, Jacqueline -- Marsland, Benjamin J -- Oxenius, Annette -- Kopf, Manfred -- New York, N.Y. -- Science. 2009 Jun 19;324(5934):1576-80. doi: 10.1126/science.1172815. Epub 2009 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biomedicine, Institute of Integrative Biology, ETH Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478140" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology ; Chronic Disease ; Humans ; Immunologic Memory ; Interferon-gamma/biosynthesis ; Lymphocytic Choriomeningitis/*immunology ; Mice ; Mice, Inbred C57BL ; Peptide Fragments/biosynthesis ; Receptors, Interleukin-21/*immunology ; 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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  • 2
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    The alarmin interleukin-33 drives protective antiviral CD8(+) T cell responses (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-11
    Description: Pathogen-associated molecular patterns decisively influence antiviral immune responses, whereas the contribution of endogenous signals of tissue damage, also known as damage-associated molecular patterns or alarmins, remains ill defined. We show that interleukin-33 (IL-33), an alarmin released from necrotic cells, is necessary for potent CD8(+) T cell (CTL) responses to replicating, prototypic RNA and DNA viruses in mice. IL-33 signaled through its receptor on activated CTLs, enhanced clonal expansion in a CTL-intrinsic fashion, determined plurifunctional effector cell differentiation, and was necessary for virus control. Moreover, recombinant IL-33 augmented vaccine-induced CTL responses. Radio-resistant cells of the splenic T cell zone produced IL-33, and efficient CTL responses required IL-33 from radio-resistant cells but not from hematopoietic cells. Thus, alarmin release by radio-resistant cells orchestrates protective antiviral CTL responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonilla, Weldy V -- Frohlich, Anja -- Senn, Karin -- Kallert, Sandra -- Fernandez, Marylise -- Johnson, Susan -- Kreutzfeldt, Mario -- Hegazy, Ahmed N -- Schrick, Christina -- Fallon, Padraic G -- Klemenz, Roman -- Nakae, Susumu -- Adler, Heiko -- Merkler, Doron -- Lohning, Max -- Pinschewer, Daniel D -- New York, N.Y. -- Science. 2012 Feb 24;335(6071):984-9. doi: 10.1126/science.1215418. Epub 2012 Feb 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, University of Geneva, 1 rue Michel Servet, 1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22323740" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Arenaviridae Infections/*immunology/pathology ; Cell Differentiation ; Gene Expression Profiling ; Herpesviridae Infections/*immunology ; Interleukin-33 ; Interleukins/genetics/immunology/*metabolism ; Lymphocyte Activation ; Lymphocytic choriomeningitis virus/*immunology/physiology ; Mice ; Mice, Transgenic ; Necrosis ; Receptors, Interleukin/genetics/metabolism ; Recombinant Proteins/immunology ; Rhadinovirus/*immunology ; Signal Transduction ; Stromal Cells/immunology/metabolism ; T-Lymphocytes, Cytotoxic/*immunology/transplantation ; Tumor Virus Infections/immunology ; Up-Regulation ; Vaccinia virus/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)
    Location Call Number Expected Availability
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