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  • Animals  (8)
  • American Association for the Advancement of Science (AAAS)  (8)
  • 1
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    Prostaglandin D2 as a mediator of allergic asthma (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-17
    Description: Allergic asthma is caused by the aberrant expansion in the lung of T helper cells that produce type 2 (TH2) cytokines and is characterized by infiltration of eosinophils and bronchial hyperreactivity. This disease is often triggered by mast cells activated by immunoglobulin E (IgE)-mediated allergic challenge. Activated mast cells release various chemical mediators, including prostaglandin D2 (PGD2), whose role in allergic asthma has now been investigated by the generation of mice deficient in the PGD receptor (DP). Sensitization and aerosol challenge of the homozygous mutant (DP-/-) mice with ovalbumin (OVA) induced increases in the serum concentration of IgE similar to those in wild-type mice subjected to this model of asthma. However, the concentrations of TH2 cytokines and the extent of lymphocyte accumulation in the lung of OVA-challenged DP-/- mice were greatly reduced compared with those in wild-type animals. Moreover, DP-/- mice showed only marginal infiltration of eosinophils and failed to develop airway hyperreactivity. Thus, PGD2 functions as a mast cell-derived mediator to trigger asthmatic responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuoka, T -- Hirata, M -- Tanaka, H -- Takahashi, Y -- Murata, T -- Kabashima, K -- Sugimoto, Y -- Kobayashi, T -- Ushikubi, F -- Aze, Y -- Eguchi, N -- Urade, Y -- Yoshida, N -- Kimura, K -- Mizoguchi, A -- Honda, Y -- Nagai, H -- Narumiya, S -- New York, N.Y. -- Science. 2000 Mar 17;287(5460):2013-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10720327" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Asthma/immunology/metabolism/pathology/*physiopathology ; Bronchial Hyperreactivity ; Bronchoalveolar Lavage Fluid/cytology/immunology ; Crosses, Genetic ; Female ; Gene Targeting ; Humans ; Immunoglobulin E/blood ; Interferon-gamma/metabolism ; Interleukins/metabolism ; Lung/immunology/metabolism/pathology ; Lymphocytes/immunology ; Male ; Mast Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Mucus/secretion ; Ovalbumin/immunology ; Prostaglandin D2/metabolism/*physiology ; *Receptors, Immunologic ; Receptors, Prostaglandin/genetics/metabolism/*physiology ; Respiratory Mucosa/secretion
    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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  • 2
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    Regulation of spermatogenesis by testis-specific, cytoplasmic poly(A) polymerase TPAP (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-10
    Description: Spermatogenesis is a highly specialized process of cellular differentiation to produce spermatozoa. This differentiation process accompanies morphological changes that are controlled by a number of genes expressed in a stage-specific manner during spermatogenesis. Here we show that in mice, the absence of a testis-specific, cytoplasmic polyadenylate [poly(A)] polymerase, TPAP, results in the arrest of spermiogenesis. TPAP-deficient mice display impaired expression of haploid-specific genes that are required for the morphogenesis of germ cells. The TPAP deficiency also causes incomplete elongation of poly(A) tails of particular transcription factor messenger RNAs. Although the overall cellular level of the transcription factor TAF10 is unaffected, TAF10 is insufficiently transported into the nucleus of germ cells. We propose that TPAP governs germ cell morphogenesis by modulating specific transcription factors at posttranscriptional and posttranslational levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kashiwabara, Shin-Ichi -- Noguchi, Junko -- Zhuang, Tiangang -- Ohmura, Ko -- Honda, Arata -- Sugiura, Shin -- Miyamoto, Kiyoko -- Takahashi, Satoru -- Inoue, Kimiko -- Ogura, Atsuo -- Baba, Tadashi -- New York, N.Y. -- Science. 2002 Dec 6;298(5600):1999-2002.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Applied Biochemistry, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba Science City, Ibaraki 305-8572, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12471261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cytoplasm/enzymology ; Female ; Gene Expression Regulation, Developmental ; Gene Targeting ; In Situ Nick-End Labeling ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Nuclear Proteins/genetics/metabolism ; Organ Size ; Poly A/metabolism ; Polynucleotide Adenylyltransferase/genetics/*metabolism ; Protein Biosynthesis ; RNA, Messenger/*metabolism ; Spermatids/physiology ; Spermatocytes/physiology ; *Spermatogenesis ; Spermatozoa/*physiology ; Testis/*enzymology/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; mRNA Cleavage and Polyadenylation Factors/genetics/metabolism
    Print ISSN: 0036-8075
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  • 3
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    A membrane receptor for retinol binding protein mediates cellular uptake of vitamin A (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-27
    Description: Vitamin A has diverse biological functions. It is transported in the blood as a complex with retinol binding protein (RBP), but the molecular mechanism by which vitamin A is absorbed by cells from the vitamin A-RBP complex is not clearly understood. We identified in bovine retinal pigment epithelium cells STRA6, a multitransmembrane domain protein, as a specific membrane receptor for RBP. STRA6 binds to RBP with high affinity and has robust vitamin A uptake activity from the vitamin A-RBP complex. It is widely expressed in embryonic development and in adult organ systems. The RBP receptor represents a major physiological mediator of cellular vitamin A uptake.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawaguchi, Riki -- Yu, Jiamei -- Honda, Jane -- Hu, Jane -- Whitelegge, Julian -- Ping, Peipei -- Wiita, Patrick -- Bok, Dean -- Sun, Hui -- 5T32EY07026/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):820-5. Epub 2007 Jan 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, David Geffen School of Medicine at UCLA, 650 Charles E. Young Drive South, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17255476" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/metabolism ; Amino Acid Sequence ; Animals ; Blood-Retinal Barrier ; COS Cells ; Cattle ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cercopithecus aethiops ; Embryonic Development ; Endocytosis ; Humans ; Molecular Sequence Data ; Mutation, Missense ; Pigment Epithelium of Eye/*metabolism ; Placenta/metabolism ; Receptors, Cell Surface/*metabolism ; Retinal Vessels/metabolism ; Retinol-Binding Proteins/*metabolism ; Spleen/metabolism ; Transfection ; Vitamin A/*metabolism
    Print ISSN: 0036-8075
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  • 4
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    Revisiting carbon flux through the ocean's twilight zone (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: The oceanic biological pump drives sequestration of carbon dioxide in the deep sea via sinking particles. Rapid biological consumption and remineralization of carbon in the "twilight zone" (depths between the euphotic zone and 1000 meters) reduce the efficiency of sequestration. By using neutrally buoyant sediment traps to sample this chronically understudied realm, we measured a transfer efficiency of sinking particulate organic carbon between 150 and 500 meters of 20 and 50% at two contrasting sites. This large variability in transfer efficiency is poorly represented in biogeochemical models. If applied globally, this is equivalent to a difference in carbon sequestration of more than 3 petagrams of carbon per year.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buesseler, Ken O -- Lamborg, Carl H -- Boyd, Philip W -- Lam, Phoebe J -- Trull, Thomas W -- Bidigare, Robert R -- Bishop, James K B -- Casciotti, Karen L -- Dehairs, Frank -- Elskens, Marc -- Honda, Makio -- Karl, David M -- Siegel, David A -- Silver, Mary W -- Steinberg, Deborah K -- Valdes, Jim -- Van Mooy, Benjamin -- Wilson, Stephanie -- New York, N.Y. -- Science. 2007 Apr 27;316(5824):567-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Marine Chemistry and Geochemistry, Woods Hole Oceanographic Institution, Woods Hole, MA 02543, USA. kbuesseler@whoi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463282" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carbon/metabolism ; Carbon Dioxide ; Copepoda/physiology ; *Ecosystem ; Food Chain ; Geologic Sediments/chemistry ; Hydrogen-Ion Concentration ; Pacific Ocean ; Phytoplankton/physiology ; *Seawater/chemistry ; Zooplankton/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
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    Induction of colonic regulatory T cells by indigenous Clostridium species (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: CD4(+) T regulatory cells (T(regs)), which express the Foxp3 transcription factor, play a critical role in the maintenance of immune homeostasis. Here, we show that in mice, T(regs) were most abundant in the colonic mucosa. The spore-forming component of indigenous intestinal microbiota, particularly clusters IV and XIVa of the genus Clostridium, promoted T(reg) cell accumulation. Colonization of mice by a defined mix of Clostridium strains provided an environment rich in transforming growth factor-beta and affected Foxp3(+) T(reg) number and function in the colon. Oral inoculation of Clostridium during the early life of conventionally reared mice resulted in resistance to colitis and systemic immunoglobulin E responses in adult mice, suggesting a new therapeutic approach to autoimmunity and allergy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969237/" 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/PMC3969237/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, Koji -- Tanoue, Takeshi -- Shima, Tatsuichiro -- Imaoka, Akemi -- Kuwahara, Tomomi -- Momose, Yoshika -- Cheng, Genhong -- Yamasaki, Sho -- Saito, Takashi -- Ohba, Yusuke -- Taniguchi, Tadatsugu -- Takeda, Kiyoshi -- Hori, Shohei -- Ivanov, Ivaylo I -- Umesaki, Yoshinori -- Itoh, Kikuji -- Honda, Kenya -- R00 DK085329/DK/NIDDK NIH HHS/ -- R01 AI052359/AI/NIAID NIH HHS/ -- R01 AI056154/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 Jan 21;331(6015):337-41. doi: 10.1126/science.1198469. Epub 2010 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205640" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Cecum/microbiology ; Cells, Cultured ; Clostridium/growth & development/*immunology ; Colitis/immunology/pathology/prevention & control ; Colon/*immunology/metabolism/*microbiology ; Feces/microbiology ; Forkhead Transcription Factors/metabolism ; Germ-Free Life ; Immunity, Innate ; Immunoglobulin E/biosynthesis ; Interleukin-10/immunology/metabolism ; Intestinal Mucosa/*immunology/metabolism ; Intestine, Small/immunology ; Metagenome ; Mice ; Mice, Inbred A ; Mice, Inbred BALB C ; Receptors, Pattern Recognition/physiology ; Specific Pathogen-Free Organisms ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/*immunology/metabolism ; Transforming Growth Factor beta/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Phosphorylation of H2A by Bub1 prevents chromosomal instability through localizing shugoshin (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Bub1 is a multi-task protein kinase required for proper chromosome segregation in eukaryotes. Impairment of Bub1 in humans may lead to chromosomal instability (CIN) or tumorigenesis. Yet, the primary cellular substrate of Bub1 has remained elusive. Here, we show that Bub1 phosphorylates the conserved serine 121 of histone H2A in fission yeast Schizosaccharomyces pombe. The h2a-SA mutant, in which all cellular H2A-S121 is replaced by alanine, phenocopies the bub1 kinase-dead mutant (bub1-KD) in losing the centromeric localization of shugoshin proteins. Artificial tethering of shugoshin to centromeres largely restores the h2a-SA or bub1-KD-related CIN defects, a function that is evolutionally conserved. Thus, Bub1 kinase creates a mark for shugoshin localization and the correct partitioning of chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawashima, Shigehiro A -- Yamagishi, Yuya -- Honda, Takashi -- Ishiguro, Kei-ichiro -- Watanabe, Yoshinori -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):172-7. doi: 10.1126/science.1180189. Epub 2009 Nov 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965387" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Centromere/*metabolism ; *Chromosomal Instability ; Chromosomal Proteins, Non-Histone/genetics/*metabolism ; *Chromosome Segregation ; Chromosomes, Fungal/metabolism ; Histones/*metabolism ; Humans ; Kinetochores/metabolism ; Meiosis ; Mice ; Mitosis ; Nucleosomes/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/genetics/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Schizosaccharomyces/cytology/genetics/*metabolism ; Schizosaccharomyces pombe Proteins/genetics/*metabolism ; Serine/metabolism
    Print ISSN: 0036-8075
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  • 7
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    MUCOSAL IMMUNOLOGY. The microbiota regulates type 2 immunity through RORgammat(+) T cells (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-07-15
    Description: Changes to the symbiotic microbiota early in life, or the absence of it, can lead to exacerbated type 2 immunity and allergic inflammations. Although it is unclear how the microbiota regulates type 2 immunity, it is a strong inducer of proinflammatory T helper 17 (T(H)17) cells and regulatory T cells (T(regs)) in the intestine. Here, we report that microbiota-induced T(regs) express the nuclear hormone receptor RORgammat and differentiate along a pathway that also leads to T(H)17 cells. In the absence of RORgammat(+) T(regs), T(H)2-driven defense against helminths is more efficient, whereas T(H)2-associated pathology is exacerbated. Thus, the microbiota regulates type 2 responses through the induction of type 3 RORgammat(+) T(regs) and T(H)17 cells and acts as a key factor in balancing immune responses at mucosal surfaces.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohnmacht, Caspar -- Park, Joo-Hong -- Cording, Sascha -- Wing, James B -- Atarashi, Koji -- Obata, Yuuki -- Gaboriau-Routhiau, Valerie -- Marques, Rute -- Dulauroy, Sophie -- Fedoseeva, Maria -- Busslinger, Meinrad -- Cerf-Bensussan, Nadine -- Boneca, Ivo G -- Voehringer, David -- Hase, Koji -- Honda, Kenya -- Sakaguchi, Shimon -- Eberl, Gerard -- New York, N.Y. -- Science. 2015 Aug 28;349(6251):989-93. doi: 10.1126/science.aac4263. Epub 2015 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Microenvironment and Immunity Unit, 75724 Paris, France. ; Laboratory of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. ; RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Kanagawa 230-0045, Japan. PRESTO, Japan Science and Technology Agency, Saitama 332-0012, Japan. ; The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. ; INSERM, U1163, Laboratory of Intestinal Immunity, Paris, France. Universite Paris Descartes-Sorbonne Paris Cite and Institut Imagine, Paris, France. INRA Micalis UMR1319, Jouy-en-Josas, France. ; Center of Allergy and Environment (ZAUM), Technische Universitat and Helmholtz Zentrum Munchen, Munich, Germany. ; Research Institute of Molecular Pathology, Vienna Biocenter, 1030 Vienna, Austria. ; INSERM, U1163, Laboratory of Intestinal Immunity, Paris, France. Universite Paris Descartes-Sorbonne Paris Cite and Institut Imagine, Paris, France. ; Institut Pasteur, Biology and Genetics of Bacterial Cell Wall, 75724 Paris, France. INSERM, Groupe Avenir, 75015 Paris, France. ; Department of Infection Biology at the Institute of Clinical Microbiology, Immunology and Hygiene, University Clinic Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany. ; RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Kanagawa 230-0045, Japan. CREST, Japan Science and Technology Agency, 4-1-8 Honcho Kawaguchi, Saitama 332-0012, Japan. ; Laboratory of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. ; Institut Pasteur, Microenvironment and Immunity Unit, 75724 Paris, France. gerard.eberl@pasteur.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26160380" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Colitis, Ulcerative/immunology ; Colon/immunology/microbiology ; Germ-Free Life ; Homeostasis ; *Immunity, Mucosal ; Intestinal Mucosa/*immunology/*microbiology ; Intestine, Small/immunology/microbiology ; Intestines/immunology/*microbiology ; Mice ; Microbiota/*immunology ; Models, Immunological ; Nematospiroides dubius ; Nuclear Receptor Subfamily 1, Group F, Member 3/*metabolism ; Specific Pathogen-Free Organisms ; Strongylida Infections/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/*immunology/metabolism ; Th17 Cells/immunology ; Th2 Cells/immunology ; Vitamin A/metabolism
    Print ISSN: 0036-8075
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  • 8
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    Helminth infection promotes colonization resistance via type 2 immunity (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-04-16
    Description: Increasing incidence of inflammatory bowel diseases, such as Crohn's disease, in developed nations is associated with changes to the microbial environment, such as decreased prevalence of helminth colonization and alterations to the gut microbiota. We find that helminth infection protects mice deficient in the Crohn's disease susceptibility gene Nod2 from intestinal abnormalities by inhibiting colonization by an inflammatory Bacteroides species. Resistance to Bacteroides colonization was dependent on type 2 immunity, which promoted the establishment of a protective microbiota enriched in Clostridiales. Additionally, we show that individuals from helminth-endemic regions harbor a similar protective microbiota and that deworming treatment reduced levels of Clostridiales and increased Bacteroidales. These results support a model of the hygiene hypothesis in which certain individuals are genetically susceptible to the consequences of a changing microbial environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramanan, Deepshika -- Bowcutt, Rowann -- Lee, Soo Ching -- Tang, Mei San -- Kurtz, Zachary D -- Ding, Yi -- Honda, Kenya -- Gause, William C -- Blaser, Martin J -- Bonneau, Richard A -- Lim, Yvonne A L -- Loke, P'ng -- Cadwell, Ken -- AI007180/AI/NIAID NIH HHS/ -- AI093811/AI/NIAID NIH HHS/ -- AI107588/AI/NIAID NIH HHS/ -- DK090989/DK/NIDDK NIH HHS/ -- DK093668/DK/NIDDK NIH HHS/ -- DK103788/DK/NIDDK NIH HHS/ -- HL123340/HL/NHLBI NIH HHS/ -- P30CA016087/CA/NCI NIH HHS/ -- UL1 TR000038/TR/NCATS NIH HHS/ -- UL1 TR00038/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):608-12. doi: 10.1126/science.aaf3229. Epub 2016 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. Sackler Institute of Graduate Biomedical Sciences, New York University School of Medicine, New York, NY 10016, USA. ; Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ; Department of Parasitology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. ; Sackler Institute of Graduate Biomedical Sciences, New York University School of Medicine, New York, NY 10016, USA. Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ; Department of Pathology, New York University Langone Medical Center, New York, NY 10016, USA. ; RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa 230-0045, Japan. Japan Agency for Medical Research and Development (AMED)-Core Research for Evolutional Science and Technology (CREST), Tokyo 100-0004, Japan. ; Center for Immunity and Inflammation, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07101, USA. ; Department of Biology, Center for Genomics and Systems Biology, New York University, New York, NY 10003, USA. Courant Institute of Mathematical Sciences, New York University, New York, NY 10012, USA. Simons Center for Data Analysis, Simons Foundation, New York, NY 10011, USA. ; Department of Parasitology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. ken.cadwell@med.nyu.edu png.loke@nyumc.org limailian@um.edu.my. ; Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ken.cadwell@med.nyu.edu png.loke@nyumc.org limailian@um.edu.my. ; Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ken.cadwell@med.nyu.edu png.loke@nyumc.org limailian@um.edu.my.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27080105" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides/*immunology ; Bacteroides Infections/*immunology ; Clostridiales/immunology ; Clostridium Infections/immunology ; Crohn Disease/*genetics/immunology ; Gastrointestinal Microbiome/*immunology ; Genetic Predisposition to Disease ; Hygiene Hypothesis ; Intestines/*immunology/microbiology/parasitology ; Mice ; Mice, Mutant Strains ; Nod2 Signaling Adaptor Protein/*genetics ; Trichuriasis/*immunology ; Trichuris/*immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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