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  • 1
    Publication Date: 1995-07-28
    Description: T cell hybridomas require the immediate-early gene NGFI-B (nur77) for T cell receptor (TCR)-mediated apoptosis, a model for negative selection of self-reactive T cells. TCR-mediated death was examined in mice bearing an NGFI-B loss-of-function mutation, either by administration of antibodies to CD3 (anti-CD3) or in two well-characterized transgenic models expressing self-reactive TCRs. Both the extent and the rate of thymocyte death were unimpaired. Anti-CD3-induced death was normal in CD4+ peripheral T cells, in which death is mediated predominantly by the Fas signaling pathway. Thus, no unique requirement for NGFI-B is observed for thymic or peripheral T cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, S L -- Wesselschmidt, R L -- Linette, G P -- Kanagawa, O -- Russell, J H -- Milbrandt, J -- P01 CA49712/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Jul 28;269(5223):532-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7624775" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Antigens, CD3/immunology/physiology ; *Apoptosis ; Cells, Cultured ; Clonal Deletion ; Crosses, Genetic ; DNA-Binding Proteins/genetics/*physiology ; Female ; Gene Targeting ; Hybridomas ; Male ; Mice ; Mice, Transgenic ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Receptors, Antigen, T-Cell, alpha-beta/*physiology ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid/genetics/*physiology ; Stem Cells ; T-Lymphocyte Subsets/cytology ; T-Lymphocytes/*cytology/immunology ; Thymus Gland/cytology ; Transcription Factors/genetics/*physiology
    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
    Publication Date: 2015-04-04
    Description: T cell immunity directed against tumor-encoded amino acid substitutions occurs in some melanoma patients. This implicates missense mutations as a source of patient-specific neoantigens. However, a systematic evaluation of these putative neoantigens as targets of antitumor immunity is lacking. Moreover, it remains unknown whether vaccination can augment such responses. We found that a dendritic cell vaccine led to an increase in naturally occurring neoantigen-specific immunity and revealed previously undetected human leukocyte antigen (HLA) class I-restricted neoantigens in patients with advanced melanoma. The presentation of neoantigens by HLA-A*02:01 in human melanoma was confirmed by mass spectrometry. Vaccination promoted a diverse neoantigen-specific T cell receptor (TCR) repertoire in terms of both TCR-beta usage and clonal composition. Our results demonstrate that vaccination directed at tumor-encoded amino acid substitutions broadens the antigenic breadth and clonal diversity of antitumor immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4549796/" 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/PMC4549796/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carreno, Beatriz M -- Magrini, Vincent -- Becker-Hapak, Michelle -- Kaabinejadian, Saghar -- Hundal, Jasreet -- Petti, Allegra A -- Ly, Amy -- Lie, Wen-Rong -- Hildebrand, William H -- Mardis, Elaine R -- Linette, Gerald P -- 5U54HG00307/HG/NHGRI NIH HHS/ -- P30 CA091842/CA/NCI NIH HHS/ -- P30 CA91842/CA/NCI NIH HHS/ -- R21 CA179695/CA/NCI NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2015 May 15;348(6236):803-8. doi: 10.1126/science.aaa3828. Epub 2015 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Oncology, Washington University School of Medicine, St. Louis, MO, USA. bcarreno@dom.wustl.edu. ; Genome Institute, Washington University School of Medicine, St. Louis, MO, USA. ; Department of Medicine, Division of Oncology, Washington University School of Medicine, St. Louis, MO, USA. ; Department of Microbiology and Immunology, University of Oklahoma Health Science Center, Oklahoma City, OK, USA. ; EMD Millipore Corporation, Billerica, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25837513" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution/immunology ; Antigen Presentation ; Antigens, Neoplasm/genetics/*immunology ; Cancer Vaccines/immunology/*therapeutic use ; Dendritic Cells/immunology/*transplantation ; HLA-A2 Antigen/genetics/*immunology ; Humans ; Immunotherapy, Active/*methods ; Melanoma/genetics/immunology/*therapy ; Monitoring, Immunologic ; Mutation ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Skin Neoplasms/genetics/immunology/*therapy ; T-Lymphocytes/*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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  • 3
    Publication Date: 1988-07-29
    Description: The binding of antigen or monoclonal antibody to the T cell receptor for antigen or the closely associated CD3 complex causes increases in the concentration of intracellular ionized calcium and subsequent cell proliferation. By measuring second messenger production in primary cultures of human immunodeficiency virus (HIV-1)--infected T cells stimulated with monoclonal antibodies specific for either CD3 or CD2, a specific impairment of membrane signaling was revealed. The HIV-1--infected T cells were unable to mobilize Ca2+ after stimulation with anti-CD3, whereas CD2-induced calcium mobilization remained intact. Furthermore, the HIV-1--infected cells proliferated poorly after CD3 stimulation, although the cells retained normal DNA synthesis in response to interleukin-2 stimulation. These results show that the signals initiated by CD2 and CD3 can be regulated independently within the same T cell; uncoupling of signal transduction after antigen-specific stimulation provides a biochemical mechanism to explain, in part, the profound immunodeficiency of patients with HIV-1 infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linette, G P -- Hartzman, R J -- Ledbetter, J A -- June, C H -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):573-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Georgetown University School of Medicine, Washington, DC 20007.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2899908" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*physiopathology ; Antibodies, Monoclonal/immunology ; Antigens, CD2 ; Antigens, CD3 ; Antigens, Differentiation/physiology ; Antigens, Differentiation, T-Lymphocyte/*physiology ; Calcium/physiology ; Hiv ; Humans ; Receptors, Antigen, T-Cell/*physiology ; Receptors, Immunologic/physiology ; T-Lymphocytes/microbiology/*physiology ; Time Factors
    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
    Publication Date: 1996-09-03
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 5
    Publication Date: 2015-04-02
    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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