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  • 1
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    Impairment of mycobacterial immunity in human interleukin-12 receptor deficiency (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: In humans, interferon gamma (IFN-gamma) receptor deficiency leads to a predisposition to mycobacterial infections and impairs the formation of mature granulomas. Interleukin-12 (IL-12) receptor deficiency was found in otherwise healthy individuals with mycobacterial infections. Mature granulomas were seen, surrounded by T cells and centered with epithelioid and multinucleated giant cells, yet reduced IFN-gamma concentrations were found to be secreted by activated natural killer and T cells. Thus, IL-12-dependent IFN-gamma secretion in humans seems essential in the control of mycobacterial infections, despite the formation of mature granulomas due to IL-12-independent IFN-gamma secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altare, F -- Durandy, A -- Lammas, D -- Emile, J F -- Lamhamedi, S -- Le Deist, F -- Drysdale, P -- Jouanguy, E -- Doffinger, R -- Bernaudin, F -- Jeppsson, O -- Gollob, J A -- Meinl, E -- Segal, A W -- Fischer, A -- Kumararatne, D -- Casanova, J L -- New York, N.Y. -- Science. 1998 May 29;280(5368):1432-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U429, Hopital Necker-Enfants Malades, Paris 75015, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9603732" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytotoxicity, Immunologic ; Female ; Granuloma/immunology ; Humans ; Hypersensitivity, Delayed ; Interferon-gamma/biosynthesis/immunology/secretion ; Interleukin-12/*immunology ; Killer Cells, Natural/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Knockout ; Mutation ; Mycobacterium avium-intracellulare Infection/*immunology ; *Mycobacterium bovis ; Pedigree ; Receptors, Interferon/genetics/immunology ; Receptors, Interleukin/deficiency/*genetics ; Receptors, Interleukin-12 ; T-Lymphocytes/immunology ; Tuberculosis/*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)
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  • 2
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    Cleavage of the BMP-4 antagonist chordin by zebrafish tolloid (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-07
    Description: Dorsoventral patterning of vertebrate and Drosophila embryos requires bone morphogenetic proteins (BMPs) and antagonists of BMP activity. The Drosophila gene tolloid encodes a metalloprotease similar to BMP-1 that interacts genetically with decapentaplegic, the Drosophila homolog of vertebrate BMP-2/4. Zebrafish embryos overexpressing a zebrafish homolog of tolloid were shown to resemble loss-of-function mutations in chordino, the zebrafish homolog of the Xenopus BMP-4 antagonist Chordin. Furthermore, Chordin was degraded by COS cells expressing Tolloid. These data suggest that Tolloid antagonizes Chordin activity by proteolytically cleaving Chordin. A conserved function for zebrafish and Drosophila Tolloid during embryogenesis is proposed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blader, P -- Rastegar, S -- Fischer, N -- Strahle, U -- New York, N.Y. -- Science. 1997 Dec 12;278(5345):1937-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (IGBMC), CNRS/INSERM/ULP, BP 163, 67404 Illkirch Cedex, C.U. de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9395394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic Protein Receptors ; Bone Morphogenetic Proteins/antagonists & inhibitors/*metabolism ; COS Cells ; Cell Lineage ; *Drosophila Proteins ; Embryo, Nonmammalian/metabolism ; Gene Expression Regulation, Developmental ; Glycoproteins/*metabolism ; Insect Proteins/genetics/*metabolism ; *Intercellular Signaling Peptides and Proteins ; RNA, Messenger/genetics/metabolism ; Receptors, Cell Surface/metabolism ; *Receptors, Growth Factor ; Signal Transduction ; Tolloid-Like Metalloproteinases ; Transfection ; Xenopus Proteins ; Zebrafish/*embryology/genetics/metabolism ; Zebrafish Proteins
    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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    Dependence of germinal center B cells on expression of CD21/CD35 for survival (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-09
    Description: Affinity-driven selection of B lymphocytes within germinal centers is critical for the development of high-affinity memory cells and host protection. To investigate the role of the CD21/CD35 coreceptor in B cell competition for follicular retention and survival within the germinal center, either Cr2+ or Cr2null lysozyme-specific transgenic B cells were adoptively transferred into normal mice immunized with duck (DEL) or turkey (TEL) lysozyme, which bind with different affinities. In mice injected with high-affinity turkey lysozyme, Cr2null B cells responded by follicular retention; however, they could not survive within germinal centers. This suggests that CD21 provides a signal independent of antigen that is required for survival of B cells in the germinal center.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, M B -- Goerg, S -- Shen, L -- Prodeus, A P -- Goodnow, C C -- Kelsoe, G -- Carroll, M C -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):582-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554848" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Amino Acid Sequence ; Animals ; B-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Survival ; Female ; Gene Expression ; Germinal Center/cytology/*immunology ; Immunization ; Lymphocyte Activation ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Muramidase/immunology ; Receptors, Antigen, B-Cell/immunology ; Receptors, Complement 3b/genetics/*immunology ; Receptors, Complement 3d/genetics/*immunology ; Spleen/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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  • 4
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    Natural and engineered disorders of lymphocyte development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-02
    Description: Mammals have evolved complex developmental pathways to generate a large repertoire of B and T lymphocytes capable of mounting effective immune responses. Analysis of natural and engineered immunodeficiencies constitutes a powerful approach to delineating these pathways and identifying the molecular sensors that couple the survival of developing lymphocytes to the achievement of successful gene rearrangements at the loci coding for B and T cell antigen receptors. Besides identifying cytokines, growth factors, and transcription factors involved in lymphocyte development, genetic analysis also makes it possible to organize most of these protagonists into gene networks that control critical events in the life of developing lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, A -- Malissen, B -- New York, N.Y. -- Science. 1998 Apr 10;280(5361):237-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM U.429, Hopital Necker-Enfants Malades 149, Rue de Sevres, 75743, Paris Cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9535646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/cytology/*immunology ; Cytokines/physiology ; Gene Rearrangement, T-Lymphocyte ; Gene Transfer Techniques ; Humans ; Immunologic Deficiency Syndromes/genetics/*immunology ; Mice ; Mutagenesis ; *Mutation ; Receptors, Antigen, B-Cell/genetics/immunology/metabolism ; Receptors, Antigen, T-Cell, alpha-beta/genetics/immunology/metabolism ; Signal Transduction ; T-Lymphocytes/cytology/*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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    Control of cell fate by a deubiquitinating enzyme encoded by the fat facets gene (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-12-15
    Description: Ubiquitin is a highly conserved polypeptide found in all eukaryotes. The major function of ubiquitin is to target proteins for complete or partial degradation by a multisubunit protein complex called the proteasome. Here, the Drosophila fat facets gene, which is required for the appropriate determination of particular cells in the fly eye, was shown to encode a ubiquitin-specific protease (Ubp), an enzyme that cleaves ubiquitin from ubiquitin-protein conjugates. The Fat facets protein (FAF) acts as a regulatory Ubp that prevents degradation of its substrate by the proteasome. Flies bearing fat facets gene mutations were used to show that a Ubp is cell type--and substrate-specific and a regulator of cell fate decisions in a multicellular organism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Y -- Baker, R T -- Fischer-Vize, J A -- New York, N.Y. -- Science. 1995 Dec 15;270(5243):1828-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Texas, Austin 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8525378" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; *Cell Differentiation/genetics ; Cysteine/metabolism ; Drosophila/embryology/enzymology/genetics ; Endopeptidases/genetics/*metabolism ; Escherichia coli ; Eye/embryology ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Oligodeoxyribonucleotides ; Recombinant Fusion Proteins/genetics/metabolism ; Ubiquitins/*metabolism ; beta-Galactosidase/genetics
    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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    DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-19
    Description: About 90 percent of human pancreatic carcinomas show allelic loss at chromosome 18q. To identify candidate tumor suppressor genes on 18q, a panel of pancreatic carcinomas were analyzed for convergent sites of homozygous deletion. Twenty-five of 84 tumors had homozygous deletions at 18q21.1, a site that excludes DCC (a candidate suppressor gene for colorectal cancer) and includes DPC4, a gene similar in sequence to a Drosophila melanogaster gene (Mad) implicated in a transforming growth factor-beta (TGF-beta)-like signaling pathway. Potentially inactivating mutations in DPC4 were identified in six of 27 pancreatic carcinomas that did not have homozygous deletions at 18q21.1. These results identify DPC4 as a candidate tumor suppressor gene whose inactivation may play a role in pancreatic and possibly other human cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hahn, S A -- Schutte, M -- Hoque, A T -- Moskaluk, C A -- da Costa, L T -- Rozenblum, E -- Weinstein, C L -- Fischer, A -- Yeo, C J -- Hruban, R H -- Kern, S E -- CA62924/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 19;271(5247):350-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8553070" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Division ; Chromosome Mapping ; *Chromosomes, Human, Pair 18 ; *DNA-Binding Proteins ; Gene Deletion ; Gene Expression ; *Genes, Tumor Suppressor ; Genetic Markers ; Humans ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasm Transplantation ; Pancreatic Neoplasms/*genetics/pathology ; Proteins/chemistry/*genetics/physiology ; Signal Transduction ; Smad4 Protein ; *Trans-Activators ; Transforming Growth Factor beta/physiology ; Transplantation, Heterologous ; Tumor Cells, Cultured
    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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    A role for CD81 in early T cell development (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-12
    Description: Early stages of T cell development are thought to include a series of coordinated interactions between thymocytes and other cells of the thymus. A monoclonal antibody specific for mouse CD81 was identified that blocked the appearance of alpha beta but not gamma delta T cells in fetal organ cultures initiated with day 14.5 thymus lobes. In reaggregation cultures with CD81-transfected fibroblasts, CD4-CD8- thymocytes differentiated into CD4+CD8+ T cells. Thus, interactions between immature thymocytes and stromal cells expressing CD81 are required and may be sufficient to induce early events associated with T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boismenu, R -- Rhein, M -- Fischer, W H -- Havran, W L -- AI32751/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 12;271(5246):198-200.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539618" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD/genetics/immunology/*physiology ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Antigens, CD81 ; Base Sequence ; CHO Cells ; Cell Differentiation ; Cricetinae ; Membrane Proteins/immunology/*physiology ; Mice ; Molecular Sequence Data ; Organ Culture Techniques ; Receptors, Antigen, T-Cell, alpha-beta/*analysis ; Receptors, Antigen, T-Cell, gamma-delta/analysis ; Stromal Cells/immunology ; T-Lymphocyte Subsets/cytology/*immunology ; Thymus Gland/cytology/*immunology ; Transfection
    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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