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  • 1
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    Deficient cellular immunity--finding and fixing the defects (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-27
    Description: The critical role of cellular immunity in resistance to infectious diseases is glaringly revealed by life-threatening infections if T cell function is disrupted by an inherited or acquired immunodeficiency. Although treatment has historically focused on infectious complications, understanding of the cellular and molecular basis of immunodeficiency and technologies useful for enhancing cellular immunity have both been rapidly evolving. A new era of molecular and cellular therapy is emerging as approaches to correct abnormal genes, the loss of T cell subpopulations, and aberrant T cell homeostasis make the transition from bench to bedside.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greenberg, P D -- Riddell, S R -- AI27757/AI/NIAID NIH HHS/ -- AI41754/AI/NIAID NIH HHS/ -- CA33084/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):546-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center and Departments of Medicine and Immunology, University of Washington, Seattle, WA 98195, USA. pgreen@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10417377" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Anti-HIV Agents/therapeutic use ; HIV Infections/*immunology/therapy ; Hematopoietic Stem Cell Transplantation ; Humans ; Immunity, Cellular ; Immunologic Deficiency Syndromes/etiology/*immunology/*therapy ; Severe Combined Immunodeficiency/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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Acquired cancer resistance to combination immunotherapy from transcriptional loss of class I HLA (2018)
    Springer Nature
    Details
    Publication Date: 2018-09-25
    Description: Acquired cancer resistance to combination immunotherapy from transcriptional loss of class I HLA Acquired cancer resistance to combination immunotherapy from transcriptional loss of class I HLA, Published online: 24 September 2018; doi:10.1038/s41467-018-06300-3 Acquired resistance is a major problem in cancer immunotherapy. Here the authors report a study of two patients with Merkel cell carcinoma under immunotherapy treatment who develop resistance after deep responses for 〉1 year and identified a novel mechanism of acquired, gene-specific transcriptional suppression of HLAs.
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 3
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    The role of B cells for in vivo T cell responses to a Friend virus-induced leukemia (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-24
    Description: B cells can function as antigen-presenting cells and accessory cells for T cell responses. This study evaluated the role of B cells in the induction of protective T cell immunity to a Friend murine leukemia virus (F-MuLV)-induced leukemia (FBL). B cell-deficient mice exhibited significantly reduced tumor-specific CD4+ helper and CD8+ cytotoxic T cell responses after priming with FBL or a recombinant vaccinia virus containing F-MuLV antigens. Moreover, these mice had diminished T cell responses to the vaccinia viral antigens. Tumor-primed T cells transferred into B cell-deficient mice effectively eradicated disseminated FBL. Thus, B cells appear necessary for efficient priming but not expression of tumor and viral T cell immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schultz, K R -- Klarnet, J P -- Gieni, R S -- HayGlass, K T -- Greenberg, P D -- CA 33084/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2118273" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD4/analysis ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/analysis ; B-Lymphocytes/*immunology ; Friend murine leukemia virus/*immunology ; Genes, MHC Class I ; Immunization, Passive ; Leukemia, Experimental/*immunology/therapy ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccinia virus/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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  • 4
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    Restoration of viral immunity in immunodeficient humans by the adoptive transfer of T cell clones (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-10
    Description: The adoptive transfer of antigen-specific T cells to establish immunity is an effective therapy for viral infections and tumors in animal models. The application of this approach to human disease would require the isolation and in vitro expansion of human antigen-specific T cells and evidence that such T cells persist and function in vivo after transfer. Cytomegalovirus-specific CD8+ cytotoxic T cell (CTL) clones could be isolated from bone marrow donors, propagated in vitro, and adoptively transferred to immunodeficient bone marrow transplant recipients. No toxicity developed and the clones provided persistent reconstitution of CD8+ cytomegalovirus-specific CTL responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riddell, S R -- Watanabe, K S -- Goodrich, J M -- Li, C R -- Agha, M E -- Greenberg, P D -- CA18029/CA/NCI NIH HHS/ -- P01 CA018029/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):238-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1352912" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD3 ; Antigens, CD8/immunology ; Antigens, Differentiation, T-Lymphocyte/immunology ; Bone Marrow Transplantation/immunology ; CD4-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Cytomegalovirus Infections/*prevention & control ; Humans ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes, Cytotoxic/*immunology ; Vaccination/*methods
    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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    Cancer immunotherapy: a treatment for the masses (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-13
    Description: Cancer immunotherapy attempts to harness the exquisite power and specificity of the immune system for the treatment of malignancy. Although cancer cells are less immunogenic than pathogens, the immune system is clearly capable of recognizing and eliminating tumor cells. However, tumors frequently interfere with the development and function of immune responses. Thus, the challenge for immunotherapy is to use advances in cellular and molecular immunology to develop strategies that effectively and safely augment antitumor responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blattman, Joseph N -- Greenberg, Philip D -- New York, N.Y. -- Science. 2004 Jul 9;305(5681):200-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15247469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/therapeutic use ; Antigen Presentation ; Antigens, Neoplasm/immunology ; Cancer Vaccines/therapeutic use ; Humans ; Immunity, Cellular ; Immunity, Innate ; *Immunotherapy ; Immunotherapy, Adoptive ; Lymphocytes, Tumor-Infiltrating/immunology ; Neoplasms/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
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Rescued tolerant CD8 T cells are preprogrammed to reestablish the tolerant state (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-24
    Description: Tolerant self-antigen-specific CD8 T cells fail to proliferate in response to antigen, thereby preventing autoimmune disease. By using an in vivo mouse model, we show that tolerant T cells proliferate and become functional under lymphopenic conditions, even in a tolerogenic environment. However, T cell rescue is only transient, with tolerance reimposed upon lymphorepletion even in the absence of tolerogen (self-antigen), challenging the prevailing paradigm that continuous antigen exposure is critical to maintain tolerance. Genome-wide messenger RNA and microRNA profiling revealed that tolerant T cells have a tolerance-specific gene profile that can be temporarily overridden under lymphopenic conditions but is inevitably reimposed, which suggests epigenetic regulation. These insights into the regulatory mechanisms that maintain or break self-tolerance may lead to new strategies for the treatment of cancer and autoimmunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3754789/" 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/PMC3754789/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schietinger, Andrea -- Delrow, Jeffrey J -- Basom, Ryan S -- Blattman, Joseph N -- Greenberg, Philip D -- K01 CA117985/CA/NCI NIH HHS/ -- P30 CA015704/CA/NCI NIH HHS/ -- P30 CA015704-35/CA/NCI NIH HHS/ -- P30 DK 56465/DK/NIDDK NIH HHS/ -- P30 DK056465/DK/NIDDK NIH HHS/ -- R01 CA033084/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Feb 10;335(6069):723-7. doi: 10.1126/science.1214277. Epub 2012 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Washington (UW), Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267581" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Autoantigens/immunology ; CD8-Positive T-Lymphocytes/*immunology/physiology/transplantation ; Cell Proliferation ; Epigenesis, Genetic ; Gene Expression Profiling ; Gene Expression Regulation ; Homeostasis ; Immunologic Memory ; Lymphocyte Activation ; Lymphocyte Count ; Lymphopenia/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; MicroRNAs/genetics/metabolism ; Oligonucleotide Array Sequence Analysis ; *Self Tolerance/genetics ; Signal Transduction ; T-Lymphocyte Subsets/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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  • 7
    Electronic Resource
    Electronic Resource
    Development of a Treatment Regimen for Human Cytomegalovirus (CMV) Infection in Bone Marrow Transplantation Recipients by Adoptive Transfer of Donor-Derived CMV-Specific T Cell Clones Expanded In Vitro (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 636 (1991), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1991.tb33450.x
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    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    DEFINITION OF ALIEN H-2 DETERMINANTS ON A FRIEND LEUKAEMIA BY ANALYSIS OF ALLOREACTIVITY OF CTL FROM PRIMARY MLC (1981)
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 8 (1981), S. 0 
    Details
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: A Friend virus-induced tumour of BALB/c (H-2d) origin, HFL/d, was examined for the expression of alien H-2 antigens. The alloantigens on HFL/d were typed by generating CTL in primary MLC with HFL/d as stimulator and measuring reactivity to targets with known H-2 antigens, and confirmed by assessing recognition of HFL/d targets by CTL generated in primary MLC with stimulators expressing known H-2 antigens. Potential cross-reactivities between alloantigens were analysed by cold-target inhibition experiments. BALB/c cells stimulated with HFL/d lysed H-2b targets, and BALB/c anti-H-2b CTL lysed HFL/d; analysis with recombinant haplotypes demonstrated both H-2Kb and H-2Db alien antigens on HFL/d. C57BL/6 (H-2b) cells stimulated with HFL/d recognized H-2Kd, H-2Dd, and an additional determinant unique to HFL/d. (BALB/c x B6)F1 cells also recognised a unique HFL/d determinant not of H-2b or H-2d origin. These unique determinants, which induced a strong cytotoxic response in primary MLC, were not shared by BALB/c or B6 tumours induced by cross-reactive FMR viruses. Thus, HFL/d expressed the K and D antigens of its strain of origin, two typed alien H-2 antigens, and at least one other untyped antigen which may represent an additional H-2 determinant. These studies further demonstrate the utility of examining the reactivity of CTL generated in primary MLC to probe for the presence of alien H-2 antigens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1744-313X.1981.tb00958.x
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  • 9
    Electronic Resource
    Electronic Resource
    Principles for Adoptive T Cell Therapy of Human Viral Diseases (1995)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Immunology 13 (1995), S. 545-586 
    Details
    ISSN: 0732-0582
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.iy.13.040195.002553
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  • 10
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    Human immunodeficiency virus type 1 infection despite prior immunization with a recombinant envelope vaccine regimen. (1996)
    National Academy of Sciences
    Details
    Publication Date: 1996-04-30
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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