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  • 1
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    Constitutive display of cryptic translation products by MHC class I molecules (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: Major histocompatibility complex (MHC) class I molecules display tens of thousands of peptides on the cell surface, derived from virtually all endogenous proteins, for inspection by cytotoxic T cells (CTLs). We show that, in normal mouse cells, MHC I molecules present a peptide encoded in the 3' "untranslated" region. Despite its rarity, the peptide elicits CTL responses and induces self-tolerance, establishing that immune surveillance extends well beyond conventional polypeptides. Furthermore, translation of this cryptic peptide occurs by a previously unknown mechanism that decodes the CUG initiation codon as leucine rather than the canonical methionine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwab, Susan R -- Li, Katy C -- Kang, Chulho -- Shastri, Nilabh -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1367-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958358" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Amino Acid Sequence ; Animals ; *Antigen Presentation ; B-Lymphocytes/metabolism ; Base Sequence ; Codon, Initiator ; Codon, Terminator ; Dendritic Cells/immunology/metabolism ; Female ; Fibroblasts/metabolism ; H-2 Antigens/*immunology ; Hybridomas ; Leucine/genetics/metabolism ; Male ; Mice ; Mice, Transgenic ; Minor Histocompatibility Antigens/genetics ; Molecular Sequence Data ; Peptides/*genetics/*immunology ; *Protein Biosynthesis ; Proteins/genetics ; Self Tolerance ; Spleen/cytology/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transfection ; Transgenes
    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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    Lymphocyte sequestration through S1P lyase inhibition and disruption of S1P gradients (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-10
    Description: Lymphocyte egress from the thymus and from peripheral lymphoid organs depends on sphingosine 1-phosphate (S1P) receptor-1 and is thought to occur in response to circulatory S1P. However, the existence of an S1P gradient between lymphoid organs and blood or lymph has not been established. To further define egress requirements, we addressed why treatment with the food colorant 2-acetyl-4-tetrahydroxybutylimidazole (THI) induces lymphopenia. We found that S1P abundance in lymphoid tissues of mice is normally low but increases more than 100-fold after THI treatment and that this treatment inhibits the S1P-degrading enzyme S1P lyase. We conclude that lymphocyte egress is mediated by S1P gradients that are established by S1P lyase activity and that the lyase may represent a novel immunosuppressant drug target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwab, Susan R -- Pereira, Joao P -- Matloubian, Mehrdad -- Xu, Ying -- Huang, Yong -- Cyster, Jason G -- AI40098/AI/NIAID NIH HHS/ -- AI45073/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 9;309(5741):1735-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0414, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16151014" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehyde-Lyases/*antagonists & inhibitors/genetics/metabolism ; Animals ; B-Lymphocytes/immunology/physiology ; Chemotaxis, Leukocyte ; Enzyme Inhibitors/pharmacology ; Food Coloring Agents/pharmacology ; Hematopoietic Stem Cells/physiology ; Imidazoles/*pharmacology ; Immunosuppressive Agents/pharmacology ; Lymph/immunology/metabolism ; Lymph Nodes/immunology ; Lymphoid Tissue/immunology/metabolism ; Lymphopenia/chemically induced ; Lysophospholipids/blood/*metabolism ; Mice ; Mice, Inbred C57BL ; Pyridoxine/analogs & derivatives/pharmacology ; RNA Interference ; Receptors, Lysosphingolipid/metabolism ; Sphingosine/*analogs & derivatives/blood/metabolism ; T-Lymphocytes/*immunology/physiology ; Thymus Gland/immunology/metabolism ; Vitamin B 6/pharmacology
    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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    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)
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  • 4
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    Promotion of lymphocyte egress into blood and lymph by distinct sources of sphingosine-1-phosphate (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-17
    Description: Lymphocytes require sphingosine-1-phosphate (S1P) receptor-1 to exit lymphoid organs, but the source(s) of extracellular S1P and whether S1P directly promotes egress are unknown. By using mice in which the two kinases that generate S1P were conditionally ablated, we find that plasma S1P is mainly hematopoietic in origin, with erythrocytes a major contributor, whereas lymph S1P is from a distinct radiation-resistant source. Lymphocyte egress from thymus and secondary lymphoid organs was markedly reduced in kinase-deficient mice. Restoration of S1P to plasma rescued egress to blood but not lymph, and the rescue required lymphocyte expression of S1P-receptor-1. Thus, separate sources provide S1P to plasma and lymph to help lymphocytes exit the low-S1P environment of lymphoid organs. Disruption of compartmentalized S1P signaling is a plausible mechanism by which S1P-receptor-1 agonists function as immunosuppressives.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pappu, Rajita -- Schwab, Susan R -- Cornelissen, Ivo -- Pereira, Joao P -- Regard, Jean B -- Xu, Ying -- Camerer, Eric -- Zheng, Yao-Wu -- Huang, Yong -- Cyster, Jason G -- Coughlin, Shaun R -- HL07731/HL/NHLBI NIH HHS/ -- R01 HL065590/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 13;316(5822):295-8. Epub 2007 Mar 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Institute, University of California, San Francisco, 600 16th Street S472D, San Francisco, CA 94143-2240, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17363629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/*metabolism ; Chemotaxis, Leukocyte/physiology ; Chromatography, Liquid ; Endothelium, Vascular ; Female ; Hematopoietic Stem Cells/metabolism ; Lymphocytes/metabolism/*physiology ; Lysophospholipids/*biosynthesis/blood/deficiency/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Phosphotransferases (Alcohol Group Acceptor)/genetics/metabolism ; Receptors, Lysosphingolipid/physiology ; Sphingosine/*analogs & derivatives/biosynthesis/blood/deficiency/physiology ; Tandem Mass Spectrometry
    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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