ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Requirement for RORgamma in thymocyte survival and lymphoid organ development (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-06
    Description: Most developing thymocytes undergo apoptosis because they cannot interact productively with molecules encoded by the major histocompatibility complex. Here, we show that mice lacking the orphan nuclear hormone receptor RORgamma lose thymic expression of the anti-apoptotic factor Bcl-xL. RORgamma thus regulates the survival of CD4+8+ thymocytes and may control the temporal window during which thymocytes can undergo positive selection. RORgamma was also required for development of lymph nodes and Peyer's patches, but not splenic follicles. In its absence, there was loss of a population of CD3-CD4+CD45+ cells that normally express RORgamma and that are likely early progenitors of lymphoid organs. Hence, RORgamma has critical functions in T cell repertoire selection and lymphoid organogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Z -- Unutmaz, D -- Zou, Y R -- Sunshine, M J -- Pierani, A -- Brenner-Morton, S -- Mebius, R E -- Littman, D R -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine and Howard Hughes Medical Institute, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; *CDC2-CDC28 Kinases ; Cell Count ; Cell Cycle ; Cell Survival ; Crosses, Genetic ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Female ; Gene Targeting ; Inhibitor of Differentiation Protein 2 ; Lymphoid Tissue/cytology/embryology/*growth & development ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics/*physiology ; *Receptors, Retinoic Acid ; *Receptors, Thyroid Hormone ; *Repressor Proteins ; T-Lymphocyte Subsets/*cytology ; Thymus Gland/*cytology ; *Transcription Factors ; bcl-X Protein
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    A cryptic sensor for HIV-1 activates antiviral innate immunity in dendritic cells (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-09-11
    Description: Dendritic cells serve a key function in host defence, linking innate detection of microbes to activation of pathogen-specific adaptive immune responses. Whether there is cell-intrinsic recognition of human immunodeficiency virus (HIV) by host innate pattern-recognition receptors and subsequent coupling to antiviral T-cell responses is not yet known. Dendritic cells are largely resistant to infection with HIV-1, but facilitate infection of co-cultured T-helper cells through a process of trans-enhancement. Here we show that, when dendritic cell resistance to infection is circumvented, HIV-1 induces dendritic cell maturation, an antiviral type I interferon response and activation of T cells. This innate response is dependent on the interaction of newly synthesized HIV-1 capsid with cellular cyclophilin A (CYPA) and the subsequent activation of the transcription factor IRF3. Because the peptidylprolyl isomerase CYPA also interacts with HIV-1 capsid to promote infectivity, our results indicate that capsid conformation has evolved under opposing selective pressures for infectivity versus furtiveness. Thus, a cell-intrinsic sensor for HIV-1 exists in dendritic cells and mediates an antiviral immune response, but it is not typically engaged owing to the absence of dendritic cell infection. The virulence of HIV-1 may be related to evasion of this response, the manipulation of which may be necessary to generate an effective HIV-1 vaccine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3051279/" 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/PMC3051279/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manel, Nicolas -- Hogstad, Brandon -- Wang, Yaming -- Levy, David E -- Unutmaz, Derya -- Littman, Dan R -- AI28900/AI/NIAID NIH HHS/ -- AI33856/AI/NIAID NIH HHS/ -- R01 AI033856/AI/NIAID NIH HHS/ -- R01 AI033856-16/AI/NIAID NIH HHS/ -- R01AI065303/AI/NIAID NIH HHS/ -- R21 AI084633/AI/NIAID NIH HHS/ -- U54-AI057158/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Sep 9;467(7312):214-7. doi: 10.1038/nature09337.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829794" target="_blank"〉PubMed〈/a〉
    Keywords: Capsid Proteins/immunology ; Cell Line ; Cyclophilin A/immunology ; Dendritic Cells/cytology/*immunology/metabolism/*virology ; HIV Infections/*immunology/virology ; HIV-1/*immunology/physiology ; Humans ; *Immunity, Innate ; Interferon Regulatory Factor-3/genetics/metabolism ; Lymphocyte Activation ; Monocytes/cytology ; T-Lymphocytes/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Turkey must end violent response to protests (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altindis, Emrah -- Alpar, M Ali -- Aksay, Emre -- Beckwith, Jonathan -- Bokel, Christian -- Curl, Robert F -- Darnell, Robert B -- Elledge, Stephen J -- Erman, Burak -- Frahm, Jens -- Goff, Stephen P -- Greengard, Paul -- Hoffmann, Roald -- Ilhan, Bayazit -- Kaslin, Jan -- Lipkin, Steven M -- Poulopoulou, Cornelia -- Raz, Erez -- Rubin, Mark A -- Salturk, Mehmet -- Schrock, Richard R -- Trautmann, Alain -- Unutmaz, Derya -- Weinstein, Harel -- Kizil, Caghan -- New York, N.Y. -- Science. 2013 Jul 19;341(6143):236. doi: 10.1126/science.341.6143.236-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23869001" target="_blank"〉PubMed〈/a〉
    Keywords: Asphyxia/*chemically induced/mortality ; Hospitalization/statistics & numerical data ; *Human Rights ; Humans ; Tear Gases/*toxicity ; Turkey ; Violence/*prevention & control ; Wounds and Injuries/etiology/mortality
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Recruitment of HIV and its receptors to dendritic cell-T cell junctions (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Monocyte-derived dendritic cells (MDDCs) can efficiently bind and transfer HIV infectivity without themselves becoming infected. Using live-cell microscopy, we found that HIV was recruited to sites of cell contact in MDDCs. Analysis of conjugates between MDDCs and T cells revealed that, in the absence of antigen-specific signaling, the HIV receptors CD4, CCR5, and CXCR4 on the T cell were recruited to the interface while the MDDCs concentrated HIV to the same region. We propose that contact between dendritic cells and T cells facilitates transmission of HIV by locally concentrating virus, receptor, and coreceptor during the formation of an infectious synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, David -- Wu, Li -- Bohks, Stacy M -- KewalRamani, Vineet N -- Unutmaz, Derya -- Hope, Thomas J -- R01 AI052051/AI/NIAID NIH HHS/ -- R01-AI47770/AI/NIAID NIH HHS/ -- R01-AI49131/AI/NIAID NIH HHS/ -- R01-AI52051/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2003 May 23;300(5623):1295-7. Epub 2003 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Illinois, Chicago, IL 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730499" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD4/metabolism ; CD4-Positive T-Lymphocytes/physiology/ultrastructure/*virology ; Cell Adhesion ; Cell Membrane/virology ; Cells, Cultured ; Coculture Techniques ; Dendritic Cells/physiology/ultrastructure/*virology ; Fluorescent Antibody Technique ; Gene Products, vpr/analysis ; Green Fluorescent Proteins ; HIV-1/*physiology ; Humans ; Intercellular Junctions/physiology/*virology ; Lipopolysaccharides/pharmacology ; Luciferases/analysis ; Luminescent Proteins/analysis ; Models, Biological ; Monocytes ; Receptors, CCR5/metabolism ; Receptors, CXCR4/metabolism ; Receptors, HIV/*metabolism ; Virion/physiology ; vpr Gene Products, Human Immunodeficiency Virus
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    CCR5 is a receptor for Staphylococcus aureus leukotoxin ED (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-12-14
    Description: Pore-forming toxins are critical virulence factors for many bacterial pathogens and are central to Staphylococcus aureus-mediated killing of host cells. S. aureus encodes pore-forming bi-component leukotoxins that are toxic towards neutrophils, but also specifically target other immune cells. Despite decades since the first description of staphylococcal leukocidal activity, the host factors responsible for the selectivity of leukotoxins towards different immune cells remain unknown. Here we identify the human immunodeficiency virus (HIV) co-receptor CCR5 as a cellular determinant required for cytotoxic targeting of subsets of myeloid cells and T lymphocytes by the S. aureus leukotoxin ED (LukED). We further demonstrate that LukED-dependent cell killing is blocked by CCR5 receptor antagonists, including the HIV drug maraviroc. Remarkably, CCR5-deficient mice are largely resistant to lethal S. aureus infection, highlighting the importance of CCR5 targeting in S. aureus pathogenesis. Thus, depletion of CCR5(+) leukocytes by LukED suggests a new immune evasion mechanism of S. aureus that can be therapeutically targeted.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536884/" 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/PMC3536884/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alonzo, Francis 3rd -- Kozhaya, Lina -- Rawlings, Stephen A -- Reyes-Robles, Tamara -- DuMont, Ashley L -- Myszka, David G -- Landau, Nathaniel R -- Unutmaz, Derya -- Torres, Victor J -- F32 AI098395/AI/NIAID NIH HHS/ -- R01 AI065303/AI/NIAID NIH HHS/ -- R01-AI065303/AI/NIAID NIH HHS/ -- R21 AI087973/AI/NIAID NIH HHS/ -- R21-AI087973/AI/NIAID NIH HHS/ -- R42-MH084372-02A1/MH/NIMH NIH HHS/ -- R56-AI091856-01A1/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Jan 3;493(7430):51-5. doi: 10.1038/nature11724. Epub 2012 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Toxins/*metabolism ; CCR5 Receptor Antagonists ; Cell Death ; Cells, Cultured ; Dendritic Cells/cytology/immunology/metabolism ; Exotoxins/*metabolism ; Female ; Humans ; Immune Evasion ; Immunologic Memory ; Jurkat Cells ; Mice ; Myeloid Cells/cytology/immunology/metabolism ; Receptors, CCR5/*metabolism ; Staphylococcus aureus/immunology/*pathogenicity ; T-Lymphocytes/cytology/immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Halofuginone inhibits TH17 cell differentiation by activating the amino acid starvation response (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: A central challenge for improving autoimmune therapy is preventing inflammatory pathology without inducing generalized immunosuppression. T helper 17 (TH17) cells, characterized by their production of interleukin-17, have emerged as important and broad mediators of autoimmunity. Here we show that the small molecule halofuginone (HF) selectively inhibits mouse and human TH17 differentiation by activating a cytoprotective signaling pathway, the amino acid starvation response (AAR). Inhibition of TH17 differentiation by HF is rescued by the addition of excess amino acids and is mimicked by AAR activation after selective amino acid depletion. HF also induces the AAR in vivo and protects mice from TH17-associated experimental autoimmune encephalomyelitis. These results indicate that the AAR pathway is a potent and selective regulator of inflammatory T cell differentiation in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803727/" 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/PMC2803727/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sundrud, Mark S -- Koralov, Sergei B -- Feuerer, Markus -- Calado, Dinis Pedro -- Kozhaya, Aimee Elhed -- Rhule-Smith, Ava -- Lefebvre, Rachel E -- Unutmaz, Derya -- Mazitschek, Ralph -- Waldner, Hanspeter -- Whitman, Malcolm -- Keller, Tracy -- Rao, Anjana -- R01 AI040127/AI/NIAID NIH HHS/ -- R01 AI040127-09/AI/NIAID NIH HHS/ -- R01 AI048213/AI/NIAID NIH HHS/ -- R01 AI048213-01/AI/NIAID NIH HHS/ -- R01 CA042471/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1334-8. doi: 10.1126/science.1172638.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School and Immune Disease Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498172" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 4/metabolism ; Amino Acids/*metabolism/pharmacology ; Animals ; Autoimmunity/drug effects ; Cell Differentiation/drug effects ; Cytokines/metabolism ; Encephalomyelitis, Autoimmune, Experimental/drug therapy/immunology ; Eukaryotic Initiation Factor-2/metabolism ; Gene Expression ; Humans ; Interleukin-17/biosynthesis/genetics ; Lymphopoiesis/drug effects ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Piperidines/*pharmacology/therapeutic use ; Protein-Serine-Threonine Kinases/metabolism ; Quinazolinones/*pharmacology/therapeutic use ; Signal Transduction ; T-Lymphocyte Subsets/cytology/*drug effects/immunology/metabolism ; T-Lymphocytes, Helper-Inducer/cytology/*drug effects/immunology/metabolism
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Nonrandom HIV-1 infection and double infection via direct and cell-mediated pathways (2004)
    National Academy of Sciences
    Details
    Publication Date: 2004-01-05
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Inhibition of primary human T cell proliferation by Helicobacter pylori vacuolating toxin (VacA) is independent of VacA effects on IL-2 secretion (2004)
    National Academy of Sciences
    Details
    Publication Date: 2004-05-05
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Expression pattern of HIV-1 coreceptors on T cells: Implications for viral transmission and lymphocyte homing (1997)
    National Academy of Sciences
    Details
    Publication Date: 1997-03-04
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    Rhesus macaque dendritic cells efficiently transmit primate lentiviruses independently of DC-SIGN (2002)
    National Academy of Sciences
    Details
    Publication Date: 2002-01-29
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...