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
    ATP drives lamina propria T(H)17 cell differentiation (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-08-22
    Description: Interleukin (IL)-17-producing CD4(+) T lymphocytes (T(H)17 cells) constitute a subset of T-helper cells involved in host defence and several immune disorders. An intriguing feature of T(H)17 cells is their selective and constitutive presence in the intestinal lamina propria. Here we show that adenosine 5'-triphosphate (ATP) that can be derived from commensal bacteria activates a unique subset of lamina propria cells, CD70(high)CD11c(low) cells, leading to the differentiation of T(H)17 cells. Germ-free mice exhibit much lower concentrations of luminal ATP, accompanied by fewer lamina propria T(H)17 cells, compared to specific-pathogen-free mice. Systemic or rectal administration of ATP into these germ-free mice results in a marked increase in the number of lamina propria T(H)17 cells. A CD70(high)CD11c(low) subset of the lamina propria cells expresses T(H)17-prone molecules, such as IL-6, IL-23p19 and transforming-growth-factor-beta-activating integrin-alphaV and -beta8, in response to ATP stimulation, and preferentially induces T(H)17 differentiation of co-cultured naive CD4(+) T cells. The critical role of ATP is further underscored by the observation that administration of ATP exacerbates a T-cell-mediated colitis model with enhanced T(H)17 differentiation. These observations highlight the importance of commensal bacteria and ATP for T(H)17 differentiation in health and disease, and offer an explanation of why T(H)17 cells specifically present in the intestinal lamina propria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, Koji -- Nishimura, Junichi -- Shima, Tatsuichiro -- Umesaki, Yoshinori -- Yamamoto, Masahiro -- Onoue, Masaharu -- Yagita, Hideo -- Ishii, Naoto -- Evans, Richard -- Honda, Kenya -- Takeda, Kiyoshi -- England -- Nature. 2008 Oct 9;455(7214):808-12. doi: 10.1038/nature07240. Epub 2008 Aug 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immune Regulation, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18716618" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism/*pharmacology ; Animals ; Antigens, CD11c/metabolism ; Antigens, CD70/metabolism ; Cell Differentiation/*drug effects ; Cells, Cultured ; Colitis/chemically induced/immunology/pathology ; Disease Models, Animal ; Feces/microbiology ; Female ; Germ-Free Life ; Immunoglobulin A/analysis/immunology ; Interleukin-17/genetics/immunology/metabolism ; Male ; Mice ; Mucous Membrane/*cytology/*drug effects/immunology/microbiology ; Receptors, Purinergic P2/metabolism ; T-Lymphocytes, Helper-Inducer/*cytology/*drug effects/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
  • 2
    facet.materialart.
    Unknown
    HMGB proteins function as universal sentinels for nucleic-acid-mediated innate immune responses (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-06
    Description: The activation of innate immune responses by nucleic acids is crucial to protective and pathological immunities and is mediated by the transmembrane Toll-like receptors (TLRs) and cytosolic receptors. However, it remains unknown whether a mechanism exists that integrates these nucleic-acid-sensing systems. Here we show that high-mobility group box (HMGB) proteins 1, 2 and 3 function as universal sentinels for nucleic acids. HMGBs bind to all immunogenic nucleic acids examined with a correlation between affinity and immunogenic potential. Hmgb1(-/-) and Hmgb2(-/-) mouse cells are defective in type-I interferon and inflammatory cytokine induction by DNA or RNA targeted to activate the cytosolic nucleic-acid-sensing receptors; cells in which the expression of all three HMGBs is suppressed show a more profound defect, accompanied by impaired activation of the transcription factors interferon regulatory factor 3 (IRF3) and nuclear factor (NF)-kappaB. The absence of HMGBs also severely impairs the activation of TLR3, TLR7 and TLR9 by their cognate nucleic acids. Our results therefore indicate a hierarchy in the nucleic-acid-mediated activation of immune responses, wherein the selective activation of nucleic-acid-sensing receptors is contingent on the more promiscuous sensing of nucleic acids by HMGBs. These findings may have implications for understanding the evolution of the innate immune system and for the treatment of immunological disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yanai, Hideyuki -- Ban, Tatsuma -- Wang, ZhiChao -- Choi, Myoung Kwon -- Kawamura, Takeshi -- Negishi, Hideo -- Nakasato, Makoto -- Lu, Yan -- Hangai, Sho -- Koshiba, Ryuji -- Savitsky, David -- Ronfani, Lorenza -- Akira, Shizuo -- Bianchi, Marco E -- Honda, Kenya -- Tamura, Tomohiko -- Kodama, Tatsuhiko -- Taniguchi, Tadatsugu -- England -- Nature. 2009 Nov 5;462(7269):99-103. doi: 10.1038/nature08512.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19890330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cytosol/immunology ; DNA/immunology ; HMGB Proteins/deficiency/genetics/*immunology/*metabolism ; HMGB1 Protein/deficiency/genetics/immunology/metabolism ; HMGB2 Protein/deficiency/genetics/immunology/metabolism ; Immunity, Innate/*immunology ; Interferon Regulatory Factor-3/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Immunological ; NF-kappa B/metabolism ; Nucleic Acids/*immunology ; Nucleotides/chemistry/immunology/metabolism ; RNA/immunology ; Signal Transduction ; Toll-Like Receptors/immunology ; Virus Diseases/immunology/virology
    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
    Gain-of-function of mutated C-CBL tumour suppressor in myeloid neoplasms (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-07-22
    Description: Acquired uniparental disomy (aUPD) is a common feature of cancer genomes, leading to loss of heterozygosity. aUPD is associated not only with loss-of-function mutations of tumour suppressor genes, but also with gain-of-function mutations of proto-oncogenes. Here we show unique gain-of-function mutations of the C-CBL (also known as CBL) tumour suppressor that are tightly associated with aUPD of the 11q arm in myeloid neoplasms showing myeloproliferative features. The C-CBL proto-oncogene, a cellular homologue of v-Cbl, encodes an E3 ubiquitin ligase and negatively regulates signal transduction of tyrosine kinases. Homozygous C-CBL mutations were found in most 11q-aUPD-positive myeloid malignancies. Although the C-CBL mutations were oncogenic in NIH3T3 cells, c-Cbl was shown to functionally and genetically act as a tumour suppressor. C-CBL mutants did not have E3 ubiquitin ligase activity, but inhibited that of wild-type C-CBL and CBL-B (also known as CBLB), leading to prolonged activation of tyrosine kinases after cytokine stimulation. c-Cbl(-/-) haematopoietic stem/progenitor cells (HSPCs) showed enhanced sensitivity to a variety of cytokines compared to c-Cbl(+/+) HSPCs, and transduction of C-CBL mutants into c-Cbl(-/-) HSPCs further augmented their sensitivities to a broader spectrum of cytokines, including stem-cell factor (SCF, also known as KITLG), thrombopoietin (TPO, also known as THPO), IL3 and FLT3 ligand (FLT3LG), indicating the presence of a gain-of-function that could not be attributed to a simple loss-of-function. The gain-of-function effects of C-CBL mutants on cytokine sensitivity of HSPCs largely disappeared in a c-Cbl(+/+) background or by co-transduction of wild-type C-CBL, which suggests the pathogenic importance of loss of wild-type C-CBL alleles found in most cases of C-CBL-mutated myeloid neoplasms. Our findings provide a new insight into a role of gain-of-function mutations of a tumour suppressor associated with aUPD in the pathogenesis of some myeloid cancer subsets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanada, Masashi -- Suzuki, Takahiro -- Shih, Lee-Yung -- Otsu, Makoto -- Kato, Motohiro -- Yamazaki, Satoshi -- Tamura, Azusa -- Honda, Hiroaki -- Sakata-Yanagimoto, Mamiko -- Kumano, Keiki -- Oda, Hideaki -- Yamagata, Tetsuya -- Takita, Junko -- Gotoh, Noriko -- Nakazaki, Kumi -- Kawamata, Norihiko -- Onodera, Masafumi -- Nobuyoshi, Masaharu -- Hayashi, Yasuhide -- Harada, Hiroshi -- Kurokawa, Mineo -- Chiba, Shigeru -- Mori, Hiraku -- Ozawa, Keiya -- Omine, Mitsuhiro -- Hirai, Hisamaru -- Nakauchi, Hiromitsu -- Koeffler, H Phillip -- Ogawa, Seishi -- 2R01CA026038-30/CA/NCI NIH HHS/ -- England -- Nature. 2009 Aug 13;460(7257):904-8. doi: 10.1038/nature08240. Epub 2009 Jul 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genomics Project, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19620960" target="_blank"〉PubMed〈/a〉
    Keywords: Allelic Imbalance ; Amino Acid Sequence ; Animals ; Base Sequence ; Chromosomes, Human, Pair 11/genetics ; Female ; *Genes, Tumor Suppressor ; Humans ; Leukemia, Myeloid/*genetics/metabolism/pathology ; Male ; Mice ; Mice, Knockout ; Mice, Nude ; Models, Molecular ; Molecular Sequence Data ; Mutant Proteins/chemistry/genetics/*metabolism ; Mutation ; NIH 3T3 Cells ; Neoplasm Transplantation ; Oncogenes/genetics ; Phosphorylation ; Protein Conformation ; Proto-Oncogene Proteins c-cbl/antagonists & ; inhibitors/chemistry/deficiency/*genetics/*metabolism ; Ubiquitination ; Uniparental Disomy/genetics ; ras Proteins/genetics/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
  • 4
    facet.materialart.
    Unknown
    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
    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
    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
    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
    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
    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...