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  • Cell Line  (23)
  • American Association for the Advancement of Science (AAAS)  (23)
  • Wiley
  • 1990-1994  (23)
  • 1980-1984
  • 1965-1969
  • 1960-1964
  • 1940-1944
  • 1993  (23)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (23)
  • Wiley
Years
  • 1990-1994  (23)
  • 1980-1984
  • 1965-1969
  • 1960-1964
  • 1940-1944
Year
  • 1
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    Genotypic and phenotypic characterization of HIV-1 patients with primary infection (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-27
    Description: Better characterization of human immunodeficiency virus-type 1 (HIV-1) in patients with primary infection has important implications for the development of an acquired immunodeficiency syndrome (AIDS) vaccine because vaccine strategies should target viral isolates with the properties of transmitted viruses. In five HIV-1 seroconverters, the viral phenotype was found to be uniformly macrophage-tropic and non-syncytium-inducing. Furthermore, the viruses were genotypically homogeneous within each patient, but a common signature sequence was not discernible among transmitted viruses. In the two cases where the sexual partners were also studied, the sequences of the transmitted viruses matched best with minor variants in the blood of the transmitters. There was also a stronger pressure to conserve sequences in gp120 than in gp41, nef, and p17, suggesting that a selective mechanism is involved in transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, T -- Mo, H -- Wang, N -- Nam, D S -- Cao, Y -- Koup, R A -- Ho, D D -- AI24030/AI/NIAID NIH HHS/ -- AI25541/AI/NIAID NIH HHS/ -- AI27742/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1179-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center, New York University School of Medicine, NY 10016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356453" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Female ; Gene Products, gag/chemistry/genetics ; Genes, Viral ; Genotype ; Giant Cells/physiology ; HIV Antigens/chemistry/genetics ; HIV Envelope Protein gp120/chemistry/*genetics ; HIV Envelope Protein gp41/chemistry/genetics ; HIV Infections/*microbiology/transmission ; HIV Seropositivity/microbiology ; HIV-1/chemistry/*genetics/*physiology ; Humans ; Macrophages ; Male ; Molecular Sequence Data ; Phenotype ; Sequence Alignment ; Sexual Partners ; *Viral Proteins ; Virus Replication ; gag Gene Products, Human Immunodeficiency Virus
    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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    Mutation of unique region of Bruton's tyrosine kinase in immunodeficient XID mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-16
    Description: The cytoplasmic tyrosine kinase, Bruton's tyrosine kinase (Btk, formerly bpk or atk), is crucial for B cell development. Loss of kinase activity results in the human immunodeficiency, X-linked agammaglobulinemia, characterized by a failure to produce B cells. In the murine X-linked immunodeficiency (XID), B cells are present but respond abnormally to activating signals. The Btk gene, btk, was mapped to the xid region of the mouse X chromosome by interspecific backcross analysis. A single conserved residue within the amino terminal unique region of Btk was mutated in XID mice. This change in xid probably interferes with normal B cell signaling mediated by Btk protein interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rawlings, D J -- Saffran, D C -- Tsukada, S -- Largaespada, D A -- Grimaldi, J C -- Cohen, L -- Mohr, R N -- Bazan, J F -- Howard, M -- Copeland, N G -- AR36834/AR/NIAMS NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):358-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332901" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*enzymology/immunology ; Base Sequence ; Cell Line ; Chromosome Mapping ; Crosses, Genetic ; Exons ; Female ; Genetic Linkage ; Immunologic Deficiency Syndromes/enzymology/*genetics/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Inbred DBA ; Mice, Mutant Strains ; Molecular Sequence Data ; Protein-Tyrosine Kinases/chemistry/*genetics/metabolism ; *X Chromosome
    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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    GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Doherty, D H -- Lile, J D -- Bektesh, S -- Collins, F -- New York, N.Y. -- Science. 1993 May 21;260(5111):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Astrocytes/cytology/drug effects ; Base Sequence ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cloning, Molecular ; Dopamine/*biosynthesis ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Mesencephalon/cytology/*drug effects/metabolism ; Molecular Sequence Data ; Molecular Weight ; *Nerve Growth Factors ; Nerve Tissue Proteins/chemistry/genetics/isolation & purification/*pharmacology ; Neuroglia/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Parkinson Disease/drug therapy ; Rats
    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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    Bcl-2 inhibition of neural death: decreased generation of reactive oxygen species (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-19
    Description: The proto-oncogene bcl-2 inhibits apoptotic and necrotic neural cell death. Expression of Bcl-2 in the GT1-7 neural cell line prevented death as a result of glutathione depletion. Intracellular reactive oxygen species and lipid peroxides rose rapidly in control cells depleted of glutathione, whereas cells expressing Bcl-2 displayed a blunted increase and complete survival. Modulation of the increase in reactive oxygen species influenced the degree of cell death. Yeast mutants null for superoxide dismutase were partially rescued by expression of Bcl-2. Thus, Bcl-2 prevents cell death by decreasing the net cellular generation of reactive oxygen species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kane, D J -- Sarafian, T A -- Anton, R -- Hahn, H -- Gralla, E B -- Valentine, J S -- Ord, T -- Bredesen, D E -- GM 28222/GM/NIGMS NIH HHS/ -- NS27812/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 19;262(5137):1274-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235659" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antioxidants/pharmacology ; Buthionine Sulfoximine ; *Cell Death ; Cell Line ; Glutathione/metabolism ; Hydroxyl Radical/metabolism ; Iron/metabolism ; Lipid Peroxidation ; Methionine Sulfoximine/analogs & derivatives/pharmacology ; Neurons/*cytology/metabolism ; Proto-Oncogene Proteins/*physiology ; Proto-Oncogene Proteins c-bcl-2 ; Reactive Oxygen Species/*metabolism ; Saccharomyces cerevisiae/growth & development/metabolism ; Superoxide Dismutase/metabolism
    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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  • 5
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    Selective inhibition of ras-dependent transformation by a farnesyltransferase inhibitor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: To acquire transforming potential, the precursor of the Ras oncoprotein must undergo farnesylation of the cysteine residue located in a carboxyl-terminal tetrapeptide. Inhibitors of the enzyme that catalyzes this modification, farnesyl protein transferase (FPTase), have therefore been suggested as anticancer agents for tumors in which Ras contributes to transformation. The tetrapeptide analog L-731,735 is a potent and selective inhibitor of FPTase in vitro. A prodrug of this compound, L-731,734, inhibited Ras processing in cells transformed with v-ras. L-731,734 decreased the ability of v-ras-transformed cells to form colonies in soft agar but had no effect on the efficiency of colony formation of cells transformed by either the v-raf or v-mos oncogenes. The results demonstrate selective inhibition of ras-dependent cell transformation with a synthetic organic inhibitor of FPTase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kohl, N E -- Mosser, S D -- deSolms, S J -- Giuliani, E A -- Pompliano, D L -- Graham, S L -- Smith, R L -- Scolnick, E M -- Oliff, A -- Gibbs, J B -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1934-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Research, Merck Research Laboratories, West Point, PA 19486.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8316833" target="_blank"〉PubMed〈/a〉
    Keywords: *Alkyl and Aryl Transferases ; Animals ; Antineoplastic Agents/chemistry/*pharmacology ; Cell Division/drug effects ; Cell Line ; Cell Transformation, Neoplastic/*drug effects ; Dipeptides/chemistry/*pharmacology ; Drug Design ; Farnesyltranstransferase ; *Genes, ras ; Oncogene Proteins/*metabolism ; Protein Prenylation/*drug effects ; Rats ; Transferases/*antagonists & inhibitors
    Print ISSN: 0036-8075
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  • 6
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    An antiviral soluble form of the LDL receptor induced by interferon (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-08
    Description: Interferons, which induce several intracellular antiviral proteins, also induce an extracellular soluble protein that inhibits vesicular stomatitis virus (VSV) infection. This 28-kilodalton soluble protein was purified to homogeneity and identified by protein sequencing as the ligand-binding domain of the human 160-kilodalton low density lipoprotein receptor (LDLR). The existence of an antiviral soluble LDLR was confirmed by immunoaffinity chromatography with monoclonal antibody to LDLR. This soluble receptor mediates most of the interferon-triggered antiviral activity against VSV, apparently by interfering with virus assembly or budding, and not by inhibiting virus attachment to cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, D G -- Tal, N -- Novick, D -- Barak, S -- Rubinstein, M -- New York, N.Y. -- Science. 1993 Oct 8;262(5131):250-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211145" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antiviral Agents/*biosynthesis/chemistry/isolation & purification ; Cell Line ; Cells, Cultured ; Chromatography, Affinity ; Culture Media, Serum-Free ; Cytopathogenic Effect, Viral ; HeLa Cells ; Humans ; Interferon-beta/pharmacology ; Interferon-gamma/*pharmacology ; Molecular Sequence Data ; Molecular Weight ; Receptors, LDL/*biosynthesis/chemistry/isolation & purification ; Solubility ; Vesicular stomatitis Indiana virus/growth & development
    Print ISSN: 0036-8075
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  • 7
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    Rescue of signaling by a chimeric protein containing the cytoplasmic domain of CD45 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-23
    Description: Surface expression of the CD45 tyrosine phosphatase is essential for the T cell antigen receptor (TCR) to couple optimally with its second messenger pathways. CD45 may be required to dephosphorylate a TCR-activated protein tyrosine kinase, which then transduces an activation signal from the TCR. A chimeric molecule that contained extracellular and transmembrane sequences from an allele of a major histocompatibility class I molecule and cytoplasmic sequences of CD45 restored TCR signaling in a CD45-deficient mutant T cell line. Thus, expression of the complex extracellular domain of CD45 is not required for the TCR to couple to its signaling machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hovis, R R -- Donovan, J A -- Musci, M A -- Motto, D G -- Goldman, F D -- Ross, S E -- Koretzky, G A -- CA56050-01/CA/NCI NIH HHS/ -- CA56843-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 23;260(5107):544-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8475387" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD45/genetics/*metabolism ; Base Sequence ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Enzyme Activation ; Humans ; Inositol Phosphates/metabolism ; Membrane Proteins/metabolism ; Molecular Sequence Data ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; *Signal Transduction ; T-Lymphocytes/*metabolism ; Transfection ; Tyrosine/metabolism
    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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  • 8
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    Uncovering of functional alternative CTLA-4 counter-receptor in B7-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: B7 delivers a costimulatory signal through CD28, resulting in interleukin-2 secretion and T cell proliferation. Blockade of this pathway results in T cell anergy. The in vivo role of B7 was evaluated with B7-deficient mice. These mice had a 70 percent decrease in costimulation of the response to alloantigen. Despite lacking B7 expression, activated B cells from these mice bound CTLA-4 and GL1 monoclonal antibody, demonstrating that alternative CTLA-4 ligand or ligands exist. These receptors are functionally important because the residual allogenic mixed lymphocyte responses were blocked by CTLA4Ig. Characterization of these CTLA-4 ligands should lead to strategies for manipulating the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freeman, G J -- Borriello, F -- Hodes, R J -- Reiser, H -- Hathcock, K S -- Laszlo, G -- McKnight, A J -- Kim, J -- Du, L -- Lombard, D B -- CA 40216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):907-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694362" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, CD80/genetics/*immunology/metabolism ; Antigens, Differentiation/immunology/*metabolism ; B-Lymphocytes/*immunology ; Base Sequence ; CTLA-4 Antigen ; Cell Line ; *Immunoconjugates ; Interleukin-2/secretion ; Isoantigens/immunology ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; T-Lymphocytes/*immunology ; Transfection
    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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  • 9
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    Alterations of a zinc finger-encoding gene, BCL-6, in diffuse large-cell lymphoma (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-29
    Description: The molecular pathogenesis of diffuse large-cell lymphoma (DLCL), the most frequent and clinically relevant type of lymphoma, is unknown. A gene was cloned from chromosomal translocations affecting band 3q27, which are common in DLCL. This gene, BCL-6, codes for a 79-kilodalton protein that is homologous with zinc finger-transcription factors. In 33 percent (13 of 39) of DLCL samples, but not in other types of lymphoid malignancies, the BCL-6 gene is truncated within its 5' noncoding sequences, suggesting that its expression is deregulated. Thus, BCL-6 may be a proto-oncogene specifically involved in the pathogenesis of DLCL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, B H -- Lista, F -- Lo Coco, F -- Knowles, D M -- Offit, K -- Chaganti, R S -- Dalla-Favera, R -- CA 44029/CA/NCI NIH HHS/ -- CA 48236/CA/NCI NIH HHS/ -- EY 06337/EY/NEI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Oct 29;262(5134):747-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235596" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Chromosomes, Human, Pair 3 ; DNA, Complementary ; DNA-Binding Proteins/genetics ; Exons ; Gene Rearrangement ; Humans ; Introns ; Lymphoma, Large B-Cell, Diffuse/*genetics ; Molecular Sequence Data ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-bcl-6 ; Proto-Oncogenes/*genetics ; Sequence Homology, Amino Acid ; Transcription Factors/genetics ; Translocation, Genetic ; Zinc Fingers/*genetics
    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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  • 10
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    MHC-restricted depletion of human myelin basic protein-reactive T cells by T cell vaccination (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Activated autoreactive T cells are potentially pathogenic and regulated by clonotypic networks. Experimental autoimmune diseases can be treated by inoculation with autoreactive T cells (T cell vaccination). In the present study, patients with multiple sclerosis were inoculated with irradiated myelin basic protein (MBP)-reactive T cells. T cell responses to the inoculates were induced to deplete circulating MBP-reactive T cells in the recipients. Regulatory T cell lines isolated from the recipients inhibited T cells used for vaccination. The cytotoxicity of the CD8+ T cell lines was restricted by major histocompatibility antigens. Thus, clonotypic interactions regulating autoreactive T cells in humans can be induced by T cell vaccination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Medaer, R -- Stinissen, P -- Hafler, D -- Raus, J -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1451-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Multiple Sclerosis Research Unit, Dr. L. Willems Instituut, Diepenbeek, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690157" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Cell Line ; Epitopes/immunology ; Female ; Humans ; *Immunotherapy, Adoptive ; Lymphocyte Activation ; Male ; Middle Aged ; Multiple Sclerosis/immunology/*therapy ; Myelin Basic Protein/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/*immunology ; Vaccination
    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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