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  • 1
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    Decoding the patterns of self and nonself by the innate immune system (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-16
    Description: The innate immune system evolved several strategies of self/nonself discrimination that are based on the recognition of molecular patterns demarcating infectious nonself, as well as normal and abnormal self. These patterns are deciphered by receptors that either induce or inhibit an immune response, depending on the meaning of these signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Medzhitov, Ruslan -- Janeway, Charles A Jr -- New York, N.Y. -- Science. 2002 Apr 12;296(5566):298-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. ruslan.medzhitov@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11951031" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/immunology ; Apoptosis ; Biological Evolution ; Complement Pathway, Alternative ; Histocompatibility Antigens Class I/immunology ; Humans ; *Immunity, Innate ; Inflammation ; Killer Cells, Natural/immunology ; Lipopolysaccharides/immunology ; Necrosis ; Peptidoglycan/immunology ; Receptors, Immunologic/immunology ; *Self Tolerance ; Sialic Acids/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)
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  • 2
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    Origin and physiological roles of inflammation (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-07-25
    Description: Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Medzhitov, Ruslan -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Jul 24;454(7203):428-35. doi: 10.1038/nature07201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, TAC S-669, 300 Cedar Street, New Haven, Connecticut 06510, USA. ruslan.medzhitov@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18650913" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological ; Animals ; Apoptosis ; Homeostasis ; Humans ; Inflammation/metabolism/pathology/*physiopathology ; Inflammation Mediators/immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    HIV immunology needs a new direction (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Medzhitov, Ruslan -- Littman, Dan -- England -- Nature. 2008 Oct 2;455(7213):591. doi: 10.1038/455591a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ruslan Medzhitov is professor of immunobiology at Yale University School of Medicine, 300 Cedar Street, New Haven, Connecticut 06520, USA. ruslan.medzhitov@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18833256" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/immunology ; Allergy and Immunology/*trends ; Animals ; HIV/*immunology ; HIV Infections/*immunology ; Humans ; Immunity, Innate/*immunology ; Mice ; Species Specificity
    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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    Regulation of spontaneous intestinal tumorigenesis through the adaptor protein MyD88 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-07
    Description: Inflammation is increasingly recognized as an important component of tumorigenesis, although the mechanisms and pathways involved are not well understood. Tumor development is regulated by products of several modifier genes, but instructions for their tumor-specific expression are currently unknown. We show that the signaling through the adaptor protein MyD88 has a critical role in spontaneous tumor development in mice with heterozygous mutation in the adenomatous polyposis coli (APC) gene. We found that MyD88-dependent signaling controls the expression of several key modifier genes of intestinal tumorigenesis and has a critical role in both spontaneous and carcinogen-induced tumor development. This study thus reveals the important role of an innate immune signaling pathway in intestinal tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rakoff-Nahoum, Seth -- Medzhitov, Ruslan -- New York, N.Y. -- Science. 2007 Jul 6;317(5834):124-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615359" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Proliferation ; Colonic Neoplasms/genetics/immunology/pathology/physiopathology ; Disease Models, Animal ; Female ; Gene Expression Regulation, Neoplastic ; Genes, APC ; Immunity, Innate ; Intestinal Neoplasms/genetics/immunology/pathology/*physiopathology ; Intestine, Large/pathology ; Intestine, Small/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88/genetics/*physiology ; *Signal Transduction
    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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  • 5
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    Regulation of adaptive immunity by the innate immune system (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-16
    Description: Twenty years after the proposal that pattern recognition receptors detect invasion by microbial pathogens, the field of immunology has witnessed several discoveries that have elucidated receptors and signaling pathways of microbial recognition systems and how they control the generation of T and B lymphocyte-mediated immune responses. However, there are still many fundamental questions that remain poorly understood, even though sometimes the answers are assumed to be known. Here, we discuss some of these questions, including the mechanisms by which pathogen-specific innate immune recognition activates antigen-specific adaptive immune responses and the roles of different types of innate immune recognition in host defense from infection and injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645875/" 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/PMC3645875/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwasaki, Akiko -- Medzhitov, Ruslan -- R01 AI054359/AI/NIAID NIH HHS/ -- R01 AI055502/AI/NIAID NIH HHS/ -- R01 AI062428/AI/NIAID NIH HHS/ -- R01 AI064705/AI/NIAID NIH HHS/ -- R01 AI081884/AI/NIAID NIH HHS/ -- R01AI054359/AI/NIAID NIH HHS/ -- R01AI055502/AI/NIAID NIH HHS/ -- R01AI064705/AI/NIAID NIH HHS/ -- R01DK071754/DK/NIDDK NIH HHS/ -- R21AI083242/AI/NIAID NIH HHS/ -- R37AI046688/AI/NIAID NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):291-5. doi: 10.1126/science.1183021.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA. akiko.iwasaki@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075244" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptive Immunity ; Animals ; Antigen-Presenting Cells/immunology ; Bacterial Infections/*immunology ; Humans ; *Immunity, Innate ; Ligands ; Receptors, Pattern Recognition/immunology/*metabolism ; Signal Transduction ; Toll-Like Receptors/immunology/metabolism ; Virus Diseases/*immunology
    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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  • 6
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    Disease tolerance as a defense strategy (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-01
    Description: The immune system protects from infections primarily by detecting and eliminating the invading pathogens; however, the host organism can also protect itself from infectious diseases by reducing the negative impact of infections on host fitness. This ability to tolerate a pathogen's presence is a distinct host defense strategy, which has been largely overlooked in animal and human studies. Introduction of the notion of "disease tolerance" into the conceptual tool kit of immunology will expand our understanding of infectious diseases and host pathogen interactions. Analysis of disease tolerance mechanisms should provide new approaches for the treatment of infections and other diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3564547/" 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/PMC3564547/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Medzhitov, Ruslan -- Schneider, David S -- Soares, Miguel P -- 1DP1OD008167-01/OD/NIH HHS/ -- R01 AI055502/AI/NIAID NIH HHS/ -- R01 DK071754/DK/NIDDK NIH HHS/ -- R01AI055502/AI/NIAID NIH HHS/ -- R01AI060164/AI/NIAID NIH HHS/ -- R01DK071754/DK/NIDDK NIH HHS/ -- R37 AI046688/AI/NIAID NIH HHS/ -- R37AI046688/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Feb 24;335(6071):936-41. doi: 10.1126/science.1214935.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA. ruslan.medzhitov@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22363001" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Disease Resistance ; Disease Susceptibility ; *Host-Pathogen Interactions ; Humans ; *Immunity, Innate ; Infection/*immunology/pathology/physiopathology ; Virulence
    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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  • 7
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    Role of tissue protection in lethal respiratory viral-bacterial coinfection (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-27
    Description: Secondary bacterial pneumonia leads to increased morbidity and mortality from influenza virus infections. What causes this increased susceptibility, however, is not well defined. Host defense from infection relies not only on immune resistance mechanisms but also on the ability to tolerate a given level of pathogen burden. Failure of either resistance or tolerance can contribute to disease severity, making it hard to distinguish their relative contribution. We employ a coinfection mouse model of influenza virus and Legionella pneumophila in which we can separate resistance and tolerance. We demonstrate that influenza virus can promote susceptibility to lethal bacterial coinfection, even when bacterial infection is controlled by the immune system. We propose that this failure of host defense is due to impaired ability to tolerate tissue damage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933032/" 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/PMC3933032/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jamieson, Amanda M -- Pasman, Lesley -- Yu, Shuang -- Gamradt, Pia -- Homer, Robert J -- Decker, Thomas -- Medzhitov, Ruslan -- AI R01 055502/AI/NIAID NIH HHS/ -- R01 046688/PHS HHS/ -- R01 AI046688/AI/NIAID NIH HHS/ -- R01 AI055502/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jun 7;340(6137):1230-4. doi: 10.1126/science.1233632. Epub 2013 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. amanda_jamieson@brown.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23618765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 1 ; Coinfection/*immunology/pathology ; Disease Models, Animal ; Host-Pathogen Interactions/immunology ; Interleukin-1beta/metabolism ; *Legionella pneumophila ; Legionnaires' Disease/*immunology/pathology ; Lung/microbiology/pathology/virology ; Mice ; Mice, Inbred C57BL ; *Orthomyxoviridae ; Orthomyxoviridae Infections/*immunology/pathology ; Pneumonia, Bacterial/*immunology/pathology ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptor 4/metabolism ; Tumor Necrosis Factor-alpha/metabolism
    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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  • 8
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    Toll pathway-dependent blockade of CD4+CD25+ T cell-mediated suppression by dendritic cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: Toll-like receptors (TLRs) control activation of adaptive immune responses by antigen-presenting cells (APCs). However, initiation of adaptive immune responses is also controlled by regulatory T cells (TR cells), which act to prevent activation of autoreactive T cells. Here we describe a second mechanism of immune induction by TLRs, which is independent of effects on costimulation. Microbial induction of the Toll pathway blocked the suppressive effect of CD4+CD25+ TR cells, allowing activation of pathogen-specific adaptive immune responses. This block of suppressor activity was dependent in part on interleukin-6, which was induced by TLRs upon recognition of microbial products.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pasare, Chandrashekhar -- Medzhitov, Ruslan -- New York, N.Y. -- Science. 2003 Feb 14;299(5609):1033-6. Epub 2003 Jan 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532024" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD/immunology/metabolism ; Antigens, Differentiation/metabolism ; Cells, Cultured ; Culture Media, Conditioned ; Dendritic Cells/*immunology/metabolism ; Dinucleoside Phosphates/immunology ; *Drosophila Proteins ; *Immune Tolerance ; Immunization ; Interleukin-6/*physiology/secretion ; Lipopolysaccharides/immunology ; Lymphocyte Activation ; Membrane Glycoproteins/*physiology ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88 ; Ovalbumin/immunology ; Receptors, Cell Surface/*physiology ; Receptors, Immunologic/metabolism ; Self Tolerance ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/*immunology ; Toll-Like Receptors
    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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  • 9
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    Regulation of phagosome maturation by signals from toll-like receptors (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-15
    Description: In higher metazoans, phagocytosis is essential in host defense against microbial pathogens and in clearance of apoptotic cells. Both microbial and apoptotic cells are delivered on a common route from phagosomes to lysosomes for degradation. Here, we found that activation of the Toll-like receptor (TLR) signaling pathway by bacteria, but not apoptotic cells, regulated phagocytosis at multiple steps including internalization and phagosome maturation. Phagocytosis of bacteria was impaired in the absence of TLR signaling. Two modes of phagosome maturation were observed, constitutive and inducible; their differential engagement depended on the ability of the cargo to trigger TLR signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blander, J Magarian -- Medzhitov, Ruslan -- AI46688/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 May 14;304(5673):1014-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15143282" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Antigens, Differentiation/metabolism ; Apoptosis ; Bacteria/*immunology/metabolism ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Escherichia coli/immunology/physiology ; Lysosomes/ultrastructure ; Macrophages/*immunology/metabolism/microbiology/ultrastructure ; Membrane Glycoproteins/genetics/*metabolism ; Mice ; Microscopy, Immunoelectron ; Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism ; Myeloid Differentiation Factor 88 ; *Phagocytosis ; Phagosomes/microbiology/*physiology/ultrastructure ; Receptors, Cell Surface/genetics/*metabolism ; Receptors, Immunologic/metabolism ; Recombinant Proteins/metabolism ; Salmonella typhimurium/immunology/physiology ; *Signal Transduction ; Staphylococcus aureus/immunology/physiology ; Toll-Like Receptors ; p38 Mitogen-Activated Protein Kinases
    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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  • 10
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    Toll-like receptor signaling pathways (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: Members of the Toll-like receptor (TLR) family recognize conserved microbial structures, such as bacterial lipopolysaccharide and viral double-stranded RNA, and activate signaling pathways that result in immune responses against microbial infections. All TLRs activate MyD88-dependent pathways to induce a core set of stereotyped responses, such as inflammation. However, individual TLRs can also induce immune responses that are tailored to a given microbial infection. Thus, these receptors are involved in both innate and adaptive immune responses. The mechanisms and components of these varied responses are only partly understood. Given the importance of TLRs in host defense, dissection of the pathways they activate has become an important emerging research focus. TLRs and their pathways are numerous; Science's Signal Transduction Knowledge Environment's TLR Connections Map provides an immediate, clear overview of the known components and relations of this complex system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barton, Gregory M -- Medzhitov, Ruslan -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1524-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, 300 Cedar Street, CABS660, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791976" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Antigens, Differentiation/metabolism ; *Immunity, Active ; *Immunity, Innate ; Infection/*immunology/metabolism ; Inflammation ; Interleukin-1 Receptor-Associated Kinases ; MAP Kinase Signaling System ; Membrane Glycoproteins/chemistry/*metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Myeloid Differentiation Factor 88 ; NF-kappa B/metabolism ; Protein Kinases/metabolism ; Protein Structure, Tertiary ; Receptors, Cell Surface/chemistry/*metabolism ; Receptors, Immunologic/metabolism ; *Signal Transduction ; Toll-Like Receptors
    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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