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  • 1
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2013
    In:  British Journal of Dermatology Vol. 169, No. 1 ( 2013-07), p. 201-204
    In: British Journal of Dermatology, Oxford University Press (OUP), Vol. 169, No. 1 ( 2013-07), p. 201-204
    Type of Medium: Online Resource
    ISSN: 0007-0963
    URL: Issue
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2013
    detail.hit.zdb_id: 2004086-6
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  • 2
    Online Resource
    Online Resource
    American Society for Clinical Investigation ; 1998
    In:  Journal of Clinical Investigation Vol. 102, No. 6 ( 1998-9-15), p. 1229-1238
    In: Journal of Clinical Investigation, American Society for Clinical Investigation, Vol. 102, No. 6 ( 1998-9-15), p. 1229-1238
    Type of Medium: Online Resource
    ISSN: 0021-9738
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 1998
    detail.hit.zdb_id: 2018375-6
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  • 3
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2003
    In:  Clinical and Experimental Immunology Vol. 103, No. 1 ( 2003-10-29), p. 24-29
    In: Clinical and Experimental Immunology, Oxford University Press (OUP), Vol. 103, No. 1 ( 2003-10-29), p. 24-29
    Abstract: Following HIV-1 infection, a number of disorders are induced in both normal T and B cells by virus products derived from infected CD4+ T cells. In the present study, we found that HIV-infected, but not uninfected, human T cell lines generated vigorous blastogenesis and proliferation of freshly isolated mouse B cells in a short-term culture. Neither human B cells nor rat B cells showed significant responses to the HIV-infected T cell lines in the present condition. The mitogenic effect of HIV-infected human T cell line requires direct cell–cell interaction between mouse B cells and HIV-infected T cell lines. Since either mitomycin c treatment or paraformaldehyde fixation of HIV-infected T cell lines resulted in complete loss of the mitogenic effect, it seems that de novo synthesized viral products are responsible for this effect. Furthermore, anti-mouse immunoglobulin antibody inhibited completely the B cell stimulation by the HIV-infected human T cell lines. Thus, surface immunoglobulin (sIg) on mouse B cells appears to be an essential molecule which transduces activation signals from HIV-infected human T cells into cytoplasm of the B cells.
    Type of Medium: Online Resource
    ISSN: 1365-2249 , 0009-9104
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    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2003
    detail.hit.zdb_id: 2020024-9
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  • 4
    Online Resource
    Online Resource
    Proceedings of the National Academy of Sciences ; 1992
    In:  Proceedings of the National Academy of Sciences Vol. 89, No. 14 ( 1992-07-15), p. 6506-6510
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 89, No. 14 ( 1992-07-15), p. 6506-6510
    Abstract: In the present report we describe a CD4+8- heat stable antigen-negative (HSA-) thymocyte subpopulation that expresses a distinguishably low density of alpha beta T-cell antigen receptors (TCRlo) from the majority of CD4+8- high-density TCR (TCRhi) mature-type thymocytes. This subpopulation appears relatively late in life. Analysis of MEL-14, Pgp-1 (CD44), ICAM-1 (CD54), and NK1.1 expression on this subpopulation revealed that the CD4+8- TCRlo population was a population having unique characteristics (MEL-14-, CD44+, ICAM-1+, and NK1.1+) compared to the CD4+8- TCRhi thymocytes, most of which are MEL-14+, CD44-, ICAM-1-, and NK1.1-. When TCR beta-chain variable region (V beta) usage was analyzed, this thymic population expressed predominantly products of V beta 7 and V beta 8.2 TCR gene families. Interestingly, cells with V beta 8.1 TCRs, which are reactive to Mls-1a antigens, were not eliminated from the CD4+8- HSA- TCRlo subpopulation but had been eliminated from the major CD4+8- HSA- TCRhi subpopulation in Mls-1a strains. A subset with a phenotype similar to the CD4+8- HSA- TCRlo thymocytes was also identified primarily in bone marrow, and this subset constituted approximately half of the CD4+ T cells in the bone marrow. The CD4+8- HSA- TCRlo cells showed extremely high proliferative responses to immobilized anti-TCR antibody but generated negligible responses to allogeneic H-2 antigens compared to the responses generated by the major CD4+8- HSA- CD3hi cells. However, the CD4+8- HSA- TCRlo cells in Mls-1b mice mounted vigorous proliferative responses to Mls-1a antigens but not in Mls-1a mice. The properties of this T-cell subset suggest that these cells belong to a lineage distinct from the major T-cell population.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
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    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 1992
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    The American Association of Immunologists ; 1993
    In:  The Journal of Immunology Vol. 151, No. 2 ( 1993-07-15), p. 546-555
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 151, No. 2 ( 1993-07-15), p. 546-555
    Abstract: Functions of CD4-8-TCR alpha beta+ thymocytes, which are characterized by predominant usage of V beta 8.2 TCR, have remained unclear. In this study, we found that the CD4-8-TCR alpha beta + thymocytes expressed NK1.1 Ag and IL-2R beta-chain but not IL-2R alpha-chain. When the CD4-8- TCR alpha beta + thymocytes were cultured in the presence of IL-2, the CD4-8-TCR alpha beta + thymocytes vigorously proliferated. After 7 days of culture in the presence of 1000 U/ml of IL-2, approximately half of the CD4-8-TCR alpha beta + thymocytes lost NK1.1 Ag. However, the remaining half of the CD4-8-TCR alpha beta + cells showed increasing levels of NK1.1 Ag and acquired killer activity against tumor cells such as YAC-1, P815, and EL-4. These cells also killed syngeneic as well as allogeneic thymocytes. The LAK activity by the NK1.1+ CD4-8-TCR alpha beta + thymocytes was not inhibited by anti-NK1.1, anti-TCR alpha beta, or anti-CD44 mAb but was partially inhibited by anti-LFA-1 mAb. These findings indicate that the CD4-8-TCR alpha beta + thymocyte population can be divided into two population on the basis of NK1.1 expression after culture in the presence of IL-2. The NK1.1 Ag expression on the cultured CD4-8-TCR alpha beta + seems to be correlated to acquisition of LAK activity, although the NK1.1 Ag itself may not be directly involved in the target cell recognition. The present data suggest that the CD4-8- TCR alpha beta + thymocyte population is a functional T cell lineage which may serve as cells of immune defense and/or immune regulation.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
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    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1993
    detail.hit.zdb_id: 1475085-5
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  • 6
    In: Annals of the Rheumatic Diseases, BMJ, Vol. 73, No. Suppl 2 ( 2014-06), p. 512.1-512
    Type of Medium: Online Resource
    ISSN: 0003-4967 , 1468-2060
    RVK:
    Language: English
    Publisher: BMJ
    Publication Date: 2014
    detail.hit.zdb_id: 1481557-6
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  • 7
    Online Resource
    Online Resource
    Rockefeller University Press ; 1996
    In:  The Journal of experimental medicine Vol. 183, No. 5 ( 1996-05-01), p. 2391-2396
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 183, No. 5 ( 1996-05-01), p. 2391-2396
    Abstract: Natural killer (NK) cells play an important role in immune response by producing interferon gamma (IFN-gamma) as well as exhibiting cytotoxic function. IFN-gamma produced by NK cells has been suggested to be involved in differentiation of T helper cells. On the other hand, the NKR-P1 molecule was recently identified as one of the important NK cell receptors, and it recognizes certain kinds of oligosaccharides on target cells and triggers NK cells for cytotoxicity. In the present study, we found that NK cells produce great amounts of IFN-gamma upon cross-linking of the NKR-P1 molecule. In contrast, stimulation of NK cells with IL-2 induced proliferation without producing IFN-gamma. Similar to NK cells, NK1.1+ T cells also produced IFN-gamma upon NKR-P1 cross-linking. NK1.1+ T cells produced IFN-gamma but not interleukin 4 (IL-4) upon NKR-P1 cross-linking, whereas they secreted both IFN-gamma and IL-4 upon T cell receptor cross-linking. These results indicate that NKR-P1 is a receptor molecule on NK and NK1.1+ T cells that induces not only cytotoxicity but also IFN-gamma production. Our findings provide a new pathway for IFN-gamma production by NK and NK1.1+ T cells through NKR-P1 molecules; it may be essential for immune regulation.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
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    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1996
    detail.hit.zdb_id: 1477240-1
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  • 8
    Online Resource
    Online Resource
    Rockefeller University Press ; 1994
    In:  The Journal of experimental medicine Vol. 180, No. 2 ( 1994-08-01), p. 423-432
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 180, No. 2 ( 1994-08-01), p. 423-432
    Abstract: Recent studies have revealed that 10-20% of CD4+8- or CD4-8- thymocyte populations contain NK1.1+ T cell receptor (TCR)-alpha/beta+ cells. This subpopulation shows characteristics that are different from NK1.1- CD4+ or NK1.1- CD8+ T cells and seems to have developed in a manner different from NK1.1- T cells. Although extensive studies have been performed on the NK1.1+ TCR-alpha/beta+ thymocytes, the physiological role of the NK1.1+ TCR-alpha/beta+ thymocytes has been totally unclear. In the present study, we found that freshly isolated NK1.1+ TCR-alpha/beta+ thymocytes, but neither whole thymocytes nor lymph node T cells, directly killed CD4+8+ thymocytes from normal syngeneic or allogeneic mice by using a long-term cytotoxic assay in which flow cytometry was used to detect the cytotoxicity. However, only weak cytotoxicity was detected against thymocytes from lpr mice on which the Fas antigen that transduces signals for apoptosis into the cells is not expressed. Furthermore, the NK1.1+ TCR-alpha/beta+ thymocytes exhibited high cytotoxicity against T lymphoma targets transfected with fas genes as compared with the parental T lymphoma targets or target cells transfected with mutated fas genes, which lack the function of transducing signals. On the other hand, NK1.1+ effector thymocytes from gld mice that carry a point mutation in Fas ligand did not kill thymocyte targets from normal mice. The present findings, thus, consistently suggest that the NK1.1+ TCR-alpha/beta+ thymocytes kill a subpopulation among CD4+8+ thymocytes via Fas antigen and in this way regulate generation of T lineage cells in the thymus.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
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    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1994
    detail.hit.zdb_id: 1477240-1
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  • 9
    In: British Journal of Dermatology, Oxford University Press (OUP), Vol. 178, No. 1 ( 2018-01), p. 272-275
    Type of Medium: Online Resource
    ISSN: 0007-0963 , 1365-2133
    URL: Issue
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 2004086-6
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  • 10
    Online Resource
    Online Resource
    Rockefeller University Press ; 1995
    In:  The Journal of Experimental Medicine Vol. 181, No. 3 ( 1995-03-01), p. 1235-1238
    In: The Journal of Experimental Medicine, Rockefeller University Press, Vol. 181, No. 3 ( 1995-03-01), p. 1235-1238
    Abstract: The expression of Fas ligand on natural killer (NK) cells and Fas-mediated cytotoxicity by NK cells was investigated. Fas ligand mRNA was expressed in freshly isolated NK cells but not in T cells. Furthermore, the Fas ligand was detected on the cell surface of NK cells by staining with soluble Fas molecule. We analyzed the cytolytic activity of NK cells against thymocyte targets from normal and lpr mice, and found that the NK cells killed thymocytes from normal mice but not from lpr mice. On the other hand, splenic T cells did not show any cytotoxicity against either of the thymocyte targets. Similarly, NK cells exhibited cytotoxicity against transfectants expressing Fas antigen but not against parental cells or transfectants expressing a mutant Fas antigen with deleted cytoplasmic region. These results demonstrated that NK cells express Fas ligand and possess the capability of killing target cells expressing Fas antigen on their surface. This finding suggests that NK cells play an important role by eliminating Fas-expressing cells either constitutively or inducibly in peripheral lymphoid organs.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
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    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1995
    detail.hit.zdb_id: 1477240-1
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