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
Filter
  • Mice, Inbred C57BL  (10)
  • Nuclear Receptor Subfamily 1, Group F, Member 3  (3)
  • 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
    TGF-beta-induced Foxp3 inhibits T(H)17 cell differentiation by antagonizing RORgammat function (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-03-28
    Description: T helper cells that produce IL-17 (T(H)17 cells) promote autoimmunity in mice and have been implicated in the pathogenesis of human inflammatory diseases. At mucosal surfaces, T(H)17 cells are thought to protect the host from infection, whereas regulatory T (T(reg)) cells control immune responses and inflammation triggered by the resident microflora. Differentiation of both cell types requires transforming growth factor-beta (TGF-beta), but depends on distinct transcription factors: RORgammat (encoded by Rorc(gammat)) for T(H)17 cells and Foxp3 for T(reg) cells. How TGF-beta regulates the differentiation of T cells with opposing activities has been perplexing. Here we demonstrate that, together with pro-inflammatory cytokines, TGF-beta orchestrates T(H)17 cell differentiation in a concentration-dependent manner. At low concentrations, TGF-beta synergizes with interleukin (IL)-6 and IL-21 (refs 9-11) to promote IL-23 receptor (Il23r) expression, favouring T(H)17 cell differentiation. High concentrations of TGF-beta repress IL23r expression and favour Foxp3+ T(reg) cells. RORgammat and Foxp3 are co-expressed in naive CD4+ T cells exposed to TGF-beta and in a subset of T cells in the small intestinal lamina propria of the mouse. In vitro, TGF-beta-induced Foxp3 inhibits RORgammat function, at least in part through their interaction. Accordingly, lamina propria T cells that co-express both transcription factors produce less IL-17 (also known as IL-17a) than those that express RORgammat alone. IL-6, IL-21 and IL-23 relieve Foxp3-mediated inhibition of RORgammat, thereby promoting T(H)17 cell differentiation. Therefore, the decision of antigen-stimulated cells to differentiate into either T(H)17 or T(reg) cells depends on the cytokine-regulated balance of RORgammat and Foxp3.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597437/" 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/PMC2597437/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Liang -- Lopes, Jared E -- Chong, Mark M W -- Ivanov, Ivaylo I -- Min, Roy -- Victora, Gabriel D -- Shen, Yuelei -- Du, Jianguang -- Rubtsov, Yuri P -- Rudensky, Alexander Y -- Ziegler, Steven F -- Littman, Dan R -- AI48779/AI/NIAID NIH HHS/ -- R01 AI048779/AI/NIAID NIH HHS/ -- R01 AI048779-05/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 May 8;453(7192):236-40. doi: 10.1038/nature06878. Epub 2008 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉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/18368049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Line ; Cells, Cultured ; Forkhead Transcription Factors/genetics/*metabolism ; Gene Expression Regulation/drug effects ; Humans ; Interleukin-17/biosynthesis/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Receptors, Interleukin/genetics/metabolism ; Receptors, Retinoic Acid/*antagonists & inhibitors/genetics/metabolism ; Receptors, Thyroid Hormone/*antagonists & inhibitors/genetics/metabolism ; T-Lymphocytes, Helper-Inducer/*cytology/*drug effects/metabolism ; Transforming Growth Factor beta/*pharmacology
    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
    A clonogenic bone marrow progenitor specific for macrophages and dendritic cells (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-03
    Description: Macrophages and dendritic cells (DCs) are crucial for immune and inflammatory responses and belong to a network of cells that has been termed the mononuclear phagocyte system (MPS). However, the origin and lineage of these cells remain poorly understood. Here, we describe the isolation and clonal analysis of a mouse bone marrow progenitor that is specific for monocytes, several macrophage subsets, and resident spleen DCs in vivo. It was also possible to recapitulate this differentiation in vitro by using treatment with the cytokines macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. Thus, macrophages and DCs appear to renew from a common progenitor, providing a cellular and molecular basis for the concept of the MPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fogg, Darin K -- Sibon, Claire -- Miled, Chaouki -- Jung, Steffen -- Aucouturier, Pierre -- Littman, Dan R -- Cumano, Ana -- Geissmann, Frederic -- A133856/PHS HHS/ -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):83-7. Epub 2005 Dec 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, Laboratory of Mononuclear Phagocyte Biology, Avenir Team, Necker Enfants Malades Institute, 75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16322423" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Separation ; Clone Cells ; Colony-Stimulating Factors/pharmacology ; Dendritic Cells/*cytology ; Flow Cytometry ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cell Transplantation ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/*cytology ; Mice ; Mice, Inbred C57BL ; Myeloid Progenitor Cells/*cytology/immunology ; Proto-Oncogene Proteins c-kit/analysis ; Receptors, Cytokine/analysis ; Receptors, HIV/analysis ; Recombinant Proteins ; Spleen/cytology
    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
    A genomic regulatory element that directs assembly and function of immune-specific AP-1-IRF complexes (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-18
    Description: Interferon regulatory factor 4 (IRF4) and IRF8 regulate B, T, macrophage, and dendritic cell differentiation. They are recruited to cis-regulatory Ets-IRF composite elements by PU.1 or Spi-B. How these IRFs target genes in most T cells is enigmatic given the absence of specific Ets partners. Chromatin immunoprecipitation sequencing in T helper 17 (T(H)17) cells reveals that IRF4 targets sequences enriched for activating protein 1 (AP-1)-IRF composite elements (AICEs) that are co-bound by BATF, an AP-1 factor required for T(H)17, B, and dendritic cell differentiation. IRF4 and BATF bind cooperatively to structurally divergent AICEs to promote gene activation and T(H)17 differentiation. The AICE motif directs assembly of IRF4 or IRF8 with BATF heterodimers and is also used in T(H)2, B, and dendritic cells. This genomic regulatory element and cognate factors appear to have evolved to integrate diverse immunomodulatory signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glasmacher, Elke -- Agrawal, Smita -- Chang, Abraham B -- Murphy, Theresa L -- Zeng, Wenwen -- Vander Lugt, Bryan -- Khan, Aly A -- Ciofani, Maria -- Spooner, Chauncey J -- Rutz, Sascha -- Hackney, Jason -- Nurieva, Roza -- Escalante, Carlos R -- Ouyang, Wenjun -- Littman, Dan R -- Murphy, Kenneth M -- Singh, Harinder -- RC1 AI087266/AI/NIAID NIH HHS/ -- RC4 AI092765/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):975-80. doi: 10.1126/science.1228309. Epub 2012 Sep 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Discovery Immunology, Genentech, Incorporated, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22983707" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic-Leucine Zipper Transcription Factors/metabolism ; Cell Differentiation/genetics ; Chromatin Immunoprecipitation ; Humans ; Immunomodulation/*genetics ; Interferon Regulatory Factors/*metabolism ; Mice ; Mice, Inbred C57BL ; *Regulatory Elements, Transcriptional ; Th17 Cells/*immunology ; Transcription Factor AP-1/*metabolism ; *Transcriptional Activation
    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
    Thymic origin of intestinal alphabeta T cells revealed by fate mapping of RORgammat+ cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-13
    Description: Intestinal intraepithelial T lymphocytes (IELs) are likely to play a key role in host mucosal immunity and, unlike other T cells, have been proposed to differentiate from local precursors rather than from thymocytes. We show here that IELs expressing the alphabeta T cell receptor are derived from precursors that express RORgammat, an orphan nuclear hormone receptor detected only in immature CD4+CD8+ thymocytes, fetal lymphoid tissue-inducer (LTi) cells, and LTi-like cells in cryptopatches within the adult intestinal lamina propria. Using cell fate mapping, we found that all intestinal alphabeta T cells are progeny of CD4+CD8+ thymocytes, indicating that the adult intestine is not a significant site for alphabeta T cell development. Our results suggest that intestinal RORgammat+ cells are local organizers of mucosal lymphoid tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eberl, Gerard -- Littman, Dan R -- New York, N.Y. -- Science. 2004 Jul 9;305(5681):248-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, 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/15247480" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Cell Lineage ; DNA-Binding Proteins/metabolism ; Hematopoietic Stem Cells/immunology/physiology ; Immunity, Mucosal ; Intestinal Mucosa/cytology/*immunology ; Lymphoid Tissue/embryology/immunology ; Mice ; Mice, Transgenic ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Receptors, Antigen, T-Cell, alpha-beta/*analysis/genetics ; Receptors, Antigen, T-Cell, gamma-delta/analysis/genetics ; Receptors, Retinoic Acid/genetics/*metabolism ; Receptors, Thyroid Hormone/genetics/*metabolism ; T-Lymphocyte Subsets/cytology/*immunology ; T-Lymphocytes/cytology/*immunology ; Thymus Gland/cytology/*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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    CD8alphaalpha-mediated survival and differentiation of CD8 memory T cell precursors (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-24
    Description: Memory T cells are long-lived antigen-experienced T cells that are generally accepted to be direct descendants of proliferating primary effector cells. However, the factors that permit selective survival of these T cells are not well established. We show that homodimeric alpha chains of the CD8 molecule (CD8alphaalpha) are transiently induced on a selected subset of CD8alphabeta+ T cells upon antigenic stimulation. These CD8alphaalpha molecules promote the survival and differentiation of activated lymphocytes into memory CD8 T cells. Thus, memory precursors can be identified among primary effector cells and are selected for survival and differentiation by CD8alphaalpha.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Madakamutil, Loui T -- Christen, Urs -- Lena, Christopher J -- Wang-Zhu, Yiran -- Attinger, Antoine -- Sundarrajan, Monisha -- Ellmeier, Wilfried -- von Herrath, Matthias G -- Jensen, Peter -- Littman, Dan R -- Cheroutre, Hilde -- AI33614/AI/NIAID NIH HHS/ -- AI50263/AI/NIAID NIH HHS/ -- AI51973/AI/NIAID NIH HHS/ -- DK54451/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 23;304(5670):590-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15105501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD8/*immunology ; Arenaviridae Infections/immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cell Differentiation ; Cell Survival ; *Immunologic Memory ; Interferon-gamma/biosynthesis ; *Lymphocyte Activation ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/immunology/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Receptors, Interleukin-7/immunology/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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Microbiota restricts trafficking of bacteria to mesenteric lymph nodes by CX(3)CR1(hi) cells (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-01-22
    Description: The intestinal microbiota has a critical role in immune system and metabolic homeostasis, but it must be tolerated by the host to avoid inflammatory responses that can damage the epithelial barrier separating the host from the luminal contents. Breakdown of this regulation and the resulting inappropriate immune response to commensals are thought to lead to the development of inflammatory bowel diseases such as Crohn's disease and ulcerative colitis. We proposed that the intestinal immune system is instructed by the microbiota to limit responses to luminal antigens. Here we demonstrate in mice that, at steady state, the microbiota inhibits the transport of both commensal and pathogenic bacteria from the lumen to a key immune inductive site, the mesenteric lymph nodes (MLNs). However, in the absence of Myd88 or under conditions of antibiotic-induced dysbiosis, non-invasive bacteria were trafficked to the MLNs in a CCR7-dependent manner, and induced both T-cell responses and IgA production. Trafficking was carried out by CX(3)CR1(hi) mononuclear phagocytes, an intestinal-cell population previously reported to be non-migratory. These findings define a central role for commensals in regulating the migration to the MLNs of CX(3)CR1(hi) mononuclear phagocytes endowed with the ability to capture luminal bacteria, thereby compartmentalizing the intestinal immune response to avoid inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711636/" 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/PMC3711636/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diehl, Gretchen E -- Longman, Randy S -- Zhang, Jing-Xin -- Breart, Beatrice -- Galan, Carolina -- Cuesta, Adolfo -- Schwab, Susan R -- Littman, Dan R -- 5P30CA016087-32/CA/NCI NIH HHS/ -- R01 AI085166/AI/NIAID NIH HHS/ -- R01AI085166/AI/NIAID NIH HHS/ -- T32 CA009161/CA/NCI NIH HHS/ -- T32 DK083256/DK/NIDDK NIH HHS/ -- T32 DK083256-02/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Feb 7;494(7435):116-20. doi: 10.1038/nature11809. Epub 2013 Jan 13.〈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. Gretchen.Diehl@med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23334413" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Antigens, Bacterial/immunology ; Cell Movement ; Dendritic Cells/cytology/immunology ; Immunity, Mucosal/drug effects/*immunology ; Immunoglobulin A/immunology ; Inflammation/immunology ; Intestinal Mucosa/cytology/immunology/microbiology ; Lymph Nodes/*immunology/*microbiology ; Mesentery/*immunology ; Metagenome/immunology/*physiology ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88/deficiency/metabolism ; Phagocytes/cytology/immunology/*metabolism/microbiology ; Phagocytosis ; Receptors, CCR7/deficiency/genetics/metabolism ; Receptors, Chemokine/*metabolism ; Salmonella/cytology/drug effects/immunology ; 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
  • 8
    facet.materialart.
    Unknown
    DDX5 and its associated lncRNA Rmrp modulate TH17 cell effector functions (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-12-18
    Description: T helper 17 (TH17) lymphocytes protect mucosal barriers from infections, but also contribute to multiple chronic inflammatory diseases. Their differentiation is controlled by RORgammat, a ligand-regulated nuclear receptor. Here we identify the RNA helicase DEAD-box protein 5 (DDX5) as a RORgammat partner that coordinates transcription of selective TH17 genes, and is required for TH17-mediated inflammatory pathologies. Surprisingly, the ability of DDX5 to interact with RORgammat and coactivate its targets depends on intrinsic RNA helicase activity and binding of a conserved nuclear long noncoding RNA (lncRNA), Rmrp, which is mutated in patients with cartilage-hair hypoplasia. A targeted Rmrp gene mutation in mice, corresponding to a gene mutation in cartilage-hair hypoplasia patients, altered lncRNA chromatin occupancy, and reduced the DDX5-RORgammat interaction and RORgammat target gene transcription. Elucidation of the link between Rmrp and the DDX5-RORgammat complex reveals a role for RNA helicases and lncRNAs in tissue-specific transcriptional regulation, and provides new opportunities for therapeutic intervention in TH17-dependent diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762670/" 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/PMC4762670/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Wendy -- Thomas, Benjamin -- Flynn, Ryan A -- Gavzy, Samuel J -- Wu, Lin -- Kim, Sangwon V -- Hall, Jason A -- Miraldi, Emily R -- Ng, Charles P -- Rigo, Frank W -- Meadows, Sarah -- Montoya, Nina R -- Herrera, Natalia G -- Domingos, Ana I -- Rastinejad, Fraydoon -- Myers, Richard M -- Fuller-Pace, Frances V -- Bonneau, Richard -- Chang, Howard Y -- Acuto, Oreste -- Littman, Dan R -- 1F30CA189514-01/CA/NCI NIH HHS/ -- F30 CA189514/CA/NCI NIH HHS/ -- P50 HG007735/HG/NHGRI NIH HHS/ -- P50-HG007735/HG/NHGRI NIH HHS/ -- R01 AI080885/AI/NIAID NIH HHS/ -- R01 AI121436/AI/NIAID NIH HHS/ -- R01 DK103358/DK/NIDDK NIH HHS/ -- R01 HG004361/HG/NHGRI NIH HHS/ -- R01AI080885/AI/NIAID NIH HHS/ -- R01DK103358/DK/NIDDK NIH HHS/ -- R01HG004361/HG/NHGRI NIH HHS/ -- T32 AI100853/AI/NIAID NIH HHS/ -- T32 CA009161/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Dec 24;528(7583):517-22. doi: 10.1038/nature16193. Epub 2015 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA. ; Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK. ; Center for Personal Dynamic Regulomes, Stanford University, Stanford, California 94305, USA. ; Center for Genomics and Systems Biology, Department of Biology, New York University, New York, New York 10003, USA. ; Courant Institute of Mathematical Sciences, Computer Science Department, New York University, New York, New York 10012, USA. ; Simons Center for Data Analysis, Simons Foundation, New York, New York 10010, USA. ; Isis Pharmaceuticals, Carlsbad, California 92010, USA. ; HudsonAlpha Institute for Biotechnology, Huntsville, Alabama 35806, USA. ; Instituto Gulbenkian de Ciencia, Oeiras 2780-156, Portugal. ; Integrative Metabolism Program, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida 32827, USA. ; Division of Cancer Research, University of Dundee, Dundee DD1 9SY, UK. ; Howard Hughes Medical 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/26675721" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/genetics/metabolism ; DEAD-box RNA Helicases/genetics/*metabolism ; Female ; Gene Expression Regulation/genetics ; Hair/abnormalities ; Hirschsprung Disease/genetics ; Humans ; Immunologic Deficiency Syndromes/genetics ; Inflammation/immunology/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mutation/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Organ Specificity ; Osteochondrodysplasias/congenital/genetics ; Protein Binding ; RNA, Long Noncoding/genetics/*metabolism ; Th17 Cells/*immunology/*metabolism ; Transcription, Genetic/genetics
    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
  • 9
    facet.materialart.
    Unknown
    Maternal retinoids control type 3 innate lymphoid cells and set the offspring immunity (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-03-29
    Description: The impact of nutritional status during fetal life on the overall health of adults has been recognized; however, dietary effects on the developing immune system are largely unknown. Development of secondary lymphoid organs occurs during embryogenesis and is considered to be developmentally programmed. Secondary lymphoid organ formation depends on a subset of type 3 innate lymphoid cells (ILC3) named lymphoid tissue inducer (LTi) cells. Here we show that mouse fetal ILC3s are controlled by cell-autonomous retinoic acid (RA) signalling in utero, which pre-sets the immune fitness in adulthood. We found that embryonic lymphoid organs contain ILC progenitors that differentiate locally into mature LTi cells. Local LTi cell differentiation was controlled by maternal retinoid intake and fetal RA signalling acting in a haematopoietic cell-autonomous manner. RA controlled LTi cell maturation upstream of the transcription factor RORgammat. Accordingly, enforced expression of Rorgt restored maturation of LTi cells with impaired RA signalling, whereas RA receptors directly regulated the Rorgt locus. Finally, we established that maternal levels of dietary retinoids control the size of secondary lymphoid organs and the efficiency of immune responses in the adult offspring. Our results reveal a molecular link between maternal nutrients and the formation of immune structures required for resistance to infection in the offspring.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van de Pavert, Serge A -- Ferreira, Manuela -- Domingues, Rita G -- Ribeiro, Helder -- Molenaar, Rosalie -- Moreira-Santos, Lara -- Almeida, Francisca F -- Ibiza, Sales -- Barbosa, Ines -- Goverse, Gera -- Labao-Almeida, Carlos -- Godinho-Silva, Cristina -- Konijn, Tanja -- Schooneman, Dennis -- O'Toole, Tom -- Mizee, Mark R -- Habani, Yasmin -- Haak, Esther -- Santori, Fabio R -- Littman, Dan R -- Schulte-Merker, Stefan -- Dzierzak, Elaine -- Simas, J Pedro -- Mebius, Reina E -- Veiga-Fernandes, Henrique -- R01 AI080885/AI/NIAID NIH HHS/ -- R01AI080885/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Apr 3;508(7494):123-7. doi: 10.1038/nature13158. Epub 2014 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular Cell Biology and Immunology, VU University Medical Center, van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands [2] Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences) and University Medical Center Utrecht, 3584 CT Utrecht, Netherlands. [3]. ; 1] Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Av. Prof. Egas Moniz, Edificio Egas Moniz, 1649-028 Lisboa, Portugal [2]. ; Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Av. Prof. Egas Moniz, Edificio Egas Moniz, 1649-028 Lisboa, Portugal. ; Department of Molecular Cell Biology and Immunology, VU University Medical Center, van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands. ; Erasmus Stem Cell Institute, Department of Cell Biology, Erasmus Medical Center, 3000 CA Rotterdam, The Netherlands. ; Howard Hughes Medical Institute, Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, USA. ; Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences) and University Medical Center Utrecht, 3584 CT Utrecht, Netherlands. ; 1] Department of Molecular Cell Biology and Immunology, VU University Medical Center, van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects/immunology ; Diet ; Female ; Fetus/drug effects/*immunology ; Immunity, Innate/drug effects/*immunology ; Lymphoid Tissue/cytology/drug effects/embryology/immunology ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Prenatal Exposure Delayed Effects/*immunology ; Receptors, Retinoic Acid/metabolism ; Signal Transduction/drug effects ; Stem Cells/cytology/drug effects/immunology ; Tretinoin/administration & dosage/*immunology/metabolism/*pharmacology
    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
  • 10
    facet.materialart.
    Unknown
    Helper T cells without CD4: control of leishmaniasis in CD4-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Expression of either the CD4 or CD8 glycoproteins discriminates two functionally distinct lineages of T lymphocytes. A null mutation in the gene encoding CD4 impairs the development of the helper cell lineage that is normally defined by CD4 expression. Infection of CD4-null mice with Leishmania has revealed a population of functional helper T cells that develops despite the absence of CD4. These CD8- alpha beta T cell receptor+ T cells are major histocompatibility complex class II-restricted and produce interferon-gamma when challenged with parasite antigens. These results indicate that T lymphocyte lineage commitment and peripheral function need not depend on the function of CD4.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Locksley, R M -- Reiner, S L -- Hatam, F -- Littman, D R -- Killeen, N -- AI30663/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1448-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143-0654.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8367726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics/*immunology ; Antigens, CD8/immunology ; Antigens, Protozoan/immunology ; B-Lymphocytes/immunology ; Base Sequence ; CD4-CD8 Ratio ; Histocompatibility Antigens Class II/immunology ; Hypersensitivity, Delayed ; Interferon-gamma/biosynthesis/immunology ; Leishmania tropica/*immunology ; Leishmaniasis, Cutaneous/*immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Oligodeoxyribonucleotides ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/*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)
    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...