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  • 1
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    Impaired prion replication in spleens of mice lacking functional follicular dendritic cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-20
    Description: In scrapie-infected mice, prions are found associated with splenic but not circulating B and T lymphocytes and in the stroma, which contains follicular dendritic cells (FDCs). Formation and maintenance of mature FDCs require the presence of B cells expressing membrane-bound lymphotoxin-alpha/beta. Treatment of mice with soluble lymphotoxin-beta receptor results in the disappearance of mature FDCs from the spleen. We show that this treatment abolishes splenic prion accumulation and retards neuroinvasion after intraperitoneal scrapie inoculation. These data provide evidence that FDCs are the principal sites for prion replication in the spleen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montrasio, F -- Frigg, R -- Glatzel, M -- Klein, M A -- Mackay, F -- Aguzzi, A -- Weissmann, C -- New York, N.Y. -- Science. 2000 May 19;288(5469):1257-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuropathology, Department of Pathology, University of Zurich, Schmelzbergstrasse 12, CH-8091 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10818004" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/genetics/immunology ; Dendritic Cells, Follicular/metabolism/*pathology/*virology ; Immunoglobulins/genetics ; Lymphotoxin beta Receptor ; Lymphotoxin-alpha/antagonists & inhibitors/genetics/immunology ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; PrPSc Proteins/administration & dosage/*biosynthesis ; Receptors, Tumor Necrosis Factor/antagonists & inhibitors/genetics/immunology ; Recombinant Fusion Proteins/administration & dosage ; Scrapie/immunology/metabolism ; Signal Transduction/genetics/immunology ; Spleen/immunology/metabolism/*pathology/*virology ; Virus Replication/genetics/*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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  • 2
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    Microbiology. Turning up the heat on Histoplasma capsulatum (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-02-24
    Description: Many fungal pathogens are opportunistic, that is, they infect individuals who have a compromised immune system. Histoplasma capsulatum is a common pathogenic fungus that lives happily inside the phagosomes of macrophages. As Klein explains in his Perspective, an important H. capsulatum virulence factor, CBP1, has been found, which mops up free calcium ions within the phagosome, enabling the yeast to live under calcium-poor conditions (Sebhgati et al.). Chelating calcium ions may also have the added benefit that when the phagosome fuses with the lysosome, destructive lysosomal enzymes that require calcium ions for activity remain inactive.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klein, B S -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1311-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Wisconsin-Madison, Madison, WI 53792, USA. bsklein@facstaff.wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11185407" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium-Binding Proteins/*genetics/*metabolism ; Cell Line ; Gene Targeting ; Genes, Fungal ; Histoplasma/genetics/growth & development/metabolism/*pathogenicity ; Histoplasmosis/microbiology ; Hydrogen-Ion Concentration ; Lung Diseases, Fungal/microbiology ; Macrophages/*microbiology ; Mice ; Mutagenesis ; Phagosomes/metabolism/microbiology ; Plasmids ; Recombination, Genetic ; Temperature ; Transformation, Genetic ; 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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  • 3
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    In silico mapping of complex disease-related traits in mice (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-06-09
    Description: Experimental murine genetic models of complex human disease show great potential for understanding human disease pathogenesis. To reduce the time required for analysis of such models from many months down to milliseconds, a computational method for predicting chromosomal regions regulating phenotypic traits and a murine database of single nucleotide polymorphisms were developed. After entry of phenotypic information obtained from inbred mouse strains, the phenotypic and genotypic information is analyzed in silico to predict the chromosomal regions regulating the phenotypic trait.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grupe, A -- Germer, S -- Usuka, J -- Aud, D -- Belknap, J K -- Klein, R F -- Ahluwalia, M K -- Higuchi, R -- Peltz, G -- 1 R01 HG02322-01/HG/NHGRI NIH HHS/ -- R01 AR044659/AR/NIAMS NIH HHS/ -- R01 AR044659-07/AR/NIAMS NIH HHS/ -- T32HG-00044/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2001 Jun 8;292(5523):1915-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Genomics, Roche Bioscience, Palo Alto, CA 94303, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11397946" target="_blank"〉PubMed〈/a〉
    Keywords: *Algorithms ; Animals ; Bone Density ; Chromosome Mapping/*methods ; Crosses, Genetic ; Databases, Factual ; *Disease Models, Animal ; Female ; Genetic Linkage ; Genotype ; Humans ; Linkage Disequilibrium ; Major Histocompatibility Complex/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Phenotype ; Polymerase Chain Reaction ; *Polymorphism, Single Nucleotide ; *Quantitative Trait, Heritable ; Software
    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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  • 4
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    Prevention of scrapie pathogenesis by transgenic expression of anti-prion protein antibodies (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-08
    Description: Variant Creutzfeldt-Jakob disease and bovine spongiform encephalopathy are initiated by extracerebral exposure to prions. Although prion transmission from extracerebral sites to the brain represents a potential target for prophylaxis, attempts at vaccination have been limited by the poor immunogenicity of prion proteins. To circumvent this, we expressed an anti-prion protein (anti-PrP) mu chain in Prnp(o/o) mice. Transgenic mice developed sustained anti-PrP titers, which were not suppressed by introduction of Prnp+ alleles. Transgene expression prevented pathogenesis of prions introduced by intraperitoneal injection in the spleen and brain. Expression of endogenous PrP (PrP(C)) in the spleen and brain was unaffected, suggesting that immunity was responsible for protection. This indicates the feasibility of immunological inhibition of prion disease in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heppner, F L -- Musahl, C -- Arrighi, I -- Klein, M A -- Rulicke, T -- Oesch, B -- Zinkernagel, R M -- Kalinke, U -- Aguzzi, A -- New York, N.Y. -- Science. 2001 Oct 5;294(5540):178-82. Epub 2001 Sep 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuropathology, Institute of Laboratory Animal Science, Institute of Experimental Immunology, University Hospital Zurich, Schmelzbergstrasse 12, CH-8091 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11546838" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/genetics ; Animals ; Antibodies/blood/*immunology ; B-Lymphocytes/immunology ; Blotting, Western ; Brain Chemistry ; Cell Separation ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Immunoglobulin M/blood/immunology ; Immunoglobulin mu-Chains/blood/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; PrPC Proteins/genetics ; PrPSc Proteins/analysis/*immunology ; Prions/genetics/*immunology ; Protein Precursors/genetics ; Scrapie/*prevention & control ; Spleen/chemistry/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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  • 5
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    Role of brain insulin receptor in control of body weight and reproduction (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-23
    Description: Insulin receptors (IRs) and insulin signaling proteins are widely distributed throughout the central nervous system (CNS). To study the physiological role of insulin signaling in the brain, we created mice with a neuron-specific disruption of the IR gene (NIRKO mice). Inactivation of the IR had no impact on brain development or neuronal survival. However, female NIRKO mice showed increased food intake, and both male and female mice developed diet-sensitive obesity with increases in body fat and plasma leptin levels, mild insulin resistance, elevated plasma insulin levels, and hypertriglyceridemia. NIRKO mice also exhibited impaired spermatogenesis and ovarian follicle maturation because of hypothalamic dysregulation of luteinizing hormone. Thus, IR signaling in the CNS plays an important role in regulation of energy disposal, fuel metabolism, and reproduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bruning, J C -- Gautam, D -- Burks, D J -- Gillette, J -- Schubert, M -- Orban, P C -- Klein, R -- Krone, W -- Muller-Wieland, D -- Kahn, C R -- DK31036/DK/NIDDK NIH HHS/ -- DK55326-01A2/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 22;289(5487):2122-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Klinik II und Poliklinik fur Innere Medizin and Center of Molecular Medicine (ZMMK) der Universitat zu Koln, Joseph Stelzmann Strasse 9, 50931 Cologne, Germany. jens.bruening@uni-koeln.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11000114" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Animals ; Blood Glucose/analysis ; *Body Weight ; Brain/*metabolism ; Eating ; Female ; Hypertriglyceridemia/etiology ; Insulin/blood/*physiology ; Insulin Resistance ; Leptin/blood ; Leuprolide/pharmacology ; Luteinizing Hormone/blood ; Male ; Mice ; Mice, Knockout ; Neurons/metabolism ; Obesity/etiology ; Ovarian Follicle/physiology ; Receptor, Insulin/genetics/*physiology ; *Reproduction ; Sex Characteristics ; Signal Transduction ; Spermatogenesis
    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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    Local hormone networks and intestinal T cell homeostasis (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-03-28
    Description: Neuroendocrine hormones of the hypothalamus-pituitary-thyroid axis can exert positive or negative immunoregulatory effects on intestinal lymphocytes. Small intestine epithelial cells were found to express receptors for thyrotropin-releasing hormone (TRH) and to be a primary source of intestine-derived thyroid-stimulating hormone (TSH). The gene for the TSH receptor (TSH-R) was expressed in intestinal T cells but not in epithelial cells, which suggested a hormone-mediated link between lymphoid and nonhematopoietic components of the intestine. Because mice with congenitally mutant TSH-R (hyt/hyt mice) have a selectively impaired intestinal T cell repertoire, TSH may be a key immunoregulatory mediator in the intestine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, J -- Whetsell, M -- Klein, J R -- DK35566/DK/NIDDK NIH HHS/ -- R01 DK035566/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1937-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Science and Mervin Bovaird Center for Studies in Molecular Biology and Biotechnology, University of Tulsa, Tulsa, OK 74104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072972" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Homeostasis ; *Immunity, Mucosal ; Intestinal Mucosa/cytology/*immunology/metabolism ; Intestine, Small/cytology/immunology/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Point Mutation ; Receptors, Thyrotropin/genetics/metabolism ; Receptors, Thyrotropin-Releasing Hormone/genetics/metabolism ; T-Lymphocyte Subsets/immunology/metabolism ; T-Lymphocytes/*immunology/metabolism ; Thyrotropin/genetics/*metabolism ; Thyrotropin-Releasing Hormone/*metabolism/pharmacology
    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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    The branching programme of mouse lung development (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-05-09
    Description: Mammalian lungs are branched networks containing thousands to millions of airways arrayed in intricate patterns that are crucial for respiration. How such trees are generated during development, and how the developmental patterning information is encoded, have long fascinated biologists and mathematicians. However, models have been limited by a lack of information on the normal sequence and pattern of branching events. Here we present the complete three-dimensional branching pattern and lineage of the mouse bronchial tree, reconstructed from an analysis of hundreds of developmental intermediates. The branching process is remarkably stereotyped and elegant: the tree is generated by three geometrically simple local modes of branching used in three different orders throughout the lung. We propose that each mode of branching is controlled by a genetically encoded subroutine, a series of local patterning and morphogenesis operations, which are themselves controlled by a more global master routine. We show that this hierarchical and modular programme is genetically tractable, and it is ideally suited to encoding and evolving the complex networks of the lung and other branched organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892995/" 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/PMC2892995/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metzger, Ross J -- Klein, Ophir D -- Martin, Gail R -- Krasnow, Mark A -- R01 CA078711/CA/NCI NIH HHS/ -- R01 CA078711-02/CA/NCI NIH HHS/ -- R01 CA078711-03/CA/NCI NIH HHS/ -- R01 CA078711-04/CA/NCI NIH HHS/ -- R01 CA078711-05/CA/NCI NIH HHS/ -- R01 HL075769/HL/NHLBI NIH HHS/ -- R01 HL075769-01/HL/NHLBI NIH HHS/ -- R01 HL075769-02/HL/NHLBI NIH HHS/ -- R01 HL075769-03/HL/NHLBI NIH HHS/ -- R01 HL075769-04/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Jun 5;453(7196):745-50. doi: 10.1038/nature07005. Epub 2008 May 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and HHMI, Stanford University School of Medicine, Stanford, California 94305-5307, USA. ross.metzger@ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18463632" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Body Patterning/genetics/*physiology ; Fibroblast Growth Factor 10/metabolism ; Intracellular Signaling Peptides and Proteins ; Lung/*anatomy & histology/cytology/*embryology/metabolism ; Membrane Proteins/metabolism ; Mice ; Models, Biological ; Organogenesis/genetics/*physiology ; Receptor, Fibroblast Growth Factor, Type 2/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Autophagy in thymic epithelium shapes the T-cell repertoire and is essential for tolerance (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-15
    Description: Recognition of self-antigen-derived epitopes presented by major histocompatibility complex class II (MHC II) molecules on thymic epithelial cells (TECs) is critical for the generation of a functional and self-tolerant CD4 T-cell repertoire. Whereas haematopoietic antigen-presenting cells generate MHC-II-peptide complexes predominantly through the processing of endocytosed polypeptides, it remains unknown if and how TECs use unconventional pathways of antigen presentation. Here we address the role of macroautophagy, a process that has recently been shown to allow for endogenous MHC II loading, in T-cell repertoire selection in the mouse thymus. In contrast to most other tissues, TECs had a high constitutive level of autophagy. Genetic interference with autophagy specifically in TECs led to altered selection of certain MHC-II-restricted T-cell specificities and resulted in severe colitis and multi-organ inflammation. Our findings indicate that autophagy focuses the MHC-II-peptide repertoire of TECs on their intracellular milieu, which notably comprises a wide array of otherwise strictly 'tissue-specific' self antigens. In doing so, it contributes to T-cell selection and is essential for the generation of a self-tolerant T-cell repertoire.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nedjic, Jelena -- Aichinger, Martin -- Emmerich, Jan -- Mizushima, Noboru -- Klein, Ludger -- England -- Nature. 2008 Sep 18;455(7211):396-400. doi: 10.1038/nature07208. Epub 2008 Aug 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology, Doktor Bohr Gasse 7, 1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18701890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cell Differentiation ; Chimera/immunology ; Colitis/genetics/immunology/metabolism ; Epithelial Cells/cytology/immunology ; Epithelium/*immunology ; Female ; Histocompatibility Antigens/immunology ; Immune Tolerance/*immunology ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/deficiency/genetics ; Receptors, Antigen, T-Cell/immunology ; Stromal Cells/cytology ; T-Lymphocytes/*cytology/*immunology ; Thymus Gland/*cytology/*immunology/transplantation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Regulatory T-cell suppressor program co-opts transcription factor IRF4 to control T(H)2 responses (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-02-03
    Description: In the course of infection or autoimmunity, particular transcription factors orchestrate the differentiation of T(H)1, T(H)2 or T(H)17 effector cells, the responses of which are limited by a distinct lineage of suppressive regulatory T cells (T(reg)). T(reg) cell differentiation and function are guided by the transcription factor Foxp3, and their deficiency due to mutations in Foxp3 results in aggressive fatal autoimmune disease associated with sharply augmented T(H)1 and T(H)2 cytokine production. Recent studies suggested that Foxp3 regulates the bulk of the Foxp3-dependent transcriptional program indirectly through a set of transcriptional regulators serving as direct Foxp3 targets. Here we show that in mouse T(reg) cells, high amounts of interferon regulatory factor-4 (IRF4), a transcription factor essential for T(H)2 effector cell differentiation, is dependent on Foxp3 expression. We proposed that IRF4 expression endows T(reg) cells with the ability to suppress T(H)2 responses. Indeed, ablation of a conditional Irf4 allele in T(reg) cells resulted in selective dysregulation of T(H)2 responses, IL4-dependent immunoglobulin isotype production, and tissue lesions with pronounced plasma cell infiltration, in contrast to the mononuclear-cell-dominated pathology typical of mice lacking T(reg) cells. Our results indicate that T(reg) cells use components of the transcriptional machinery, promoting a particular type of effector CD4(+) T cell differentiation, to efficiently restrain the corresponding type of the immune response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864791/" 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/PMC2864791/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, Ye -- Chaudhry, Ashutosh -- Kas, Arnold -- deRoos, Paul -- Kim, Jeong M -- Chu, Tin-Tin -- Corcoran, Lynn -- Treuting, Piper -- Klein, Ulf -- Rudensky, Alexander Y -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Mar 19;458(7236):351-6. doi: 10.1038/nature07674. Epub 2009 Feb 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19182775" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/pathology ; CD4 Lymphocyte Count ; Cell Differentiation ; Forkhead Transcription Factors/deficiency/genetics/metabolism ; Immunoglobulin E/blood/immunology ; Immunoglobulin G/blood/immunology ; Interferon Regulatory Factors/deficiency/genetics/*metabolism ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes, Regulatory/*immunology ; Th2 Cells/cytology/*immunology/metabolism ; Thymus Gland/cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    TCR-peptide-MHC interactions in situ show accelerated kinetics and increased affinity (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-02-19
    Description: The recognition of foreign antigens by T lymphocytes is essential to most adaptive immune responses. It is driven by specific T-cell antigen receptors (TCRs) binding to antigenic peptide-major histocompatibility complex (pMHC) molecules on other cells. If productive, these interactions promote the formation of an immunological synapse. Here we show that synaptic TCR-pMHC binding dynamics differ significantly from TCR-pMHC binding in solution. We used single-molecule microscopy and fluorescence resonance energy transfer (FRET) between fluorescently tagged TCRs and their cognate pMHC ligands to measure the kinetics of TCR-pMHC binding in situ. When compared with solution measurements, the dissociation of this complex was increased significantly (4-12-fold). Disruption of actin polymers reversed this effect, indicating that cytoskeletal dynamics destabilize this interaction directly or indirectly. Nevertheless, TCR affinity for pMHC was significantly elevated as the result of a large (about 100-fold) increase in the association rate, a likely consequence of complementary molecular orientation and clustering. In helper T cells, the CD4 molecule has been proposed to bind cooperatively with the TCR to the same pMHC complex. However, CD4 blockade had no effect on the synaptic TCR affinity, nor did it destabilize TCR-pMHC complexes, indicating that the TCR binds pMHC independently of CD4.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273423/" 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/PMC3273423/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huppa, Johannes B -- Axmann, Markus -- Mortelmaier, Manuel A -- Lillemeier, Bjorn F -- Newell, Evan W -- Brameshuber, Mario -- Klein, Lawrence O -- Schutz, Gerhard J -- Davis, Mark M -- R0 AI52211/AI/NIAID NIH HHS/ -- R01 AI022511/AI/NIAID NIH HHS/ -- R01 AI022511-23/AI/NIAID NIH HHS/ -- R01 AI022511-27/AI/NIAID NIH HHS/ -- T32 AI007290/AI/NIAID NIH HHS/ -- Y 250/Austrian Science Fund FWF/Austria -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Feb 18;463(7283):963-7. doi: 10.1038/nature08746.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford School of Medicine, California 94305-5323, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20164930" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Antigens, CD4/drug effects/metabolism ; Cell Line ; Cells, Cultured ; Cytoskeleton/metabolism ; Drosophila melanogaster ; Fluorescence Resonance Energy Transfer ; Fluorescent Dyes ; Histocompatibility Antigens Class I/immunology/*metabolism ; Immunological Synapses/drug effects/*immunology/*metabolism ; Kinetics ; Ligands ; Mice ; Mice, Transgenic ; Peptides/*immunology/*metabolism ; Protein Binding/drug effects ; Receptors, Antigen, T-Cell/immunology/*metabolism ; Signal Transduction ; Surface Plasmon Resonance ; T-Lymphocytes, Helper-Inducer/drug effects/immunology/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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