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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 15 (1988), S. 0 
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Two hybrid cell lines expressing human CD4 were prepared by fusing human B-lymphoid cells with the mouse T-lymphoma BW5147. Hybrid TF42 was derived from a human B-lymphoblastoid line and TF53.1 from a human B-ALL. Variants of these hybrids expressing or lacking CD4 were isolated by sorting cells stained with the monoclonal antibody (mAb) OKT4 on a fluorescence-activated cell sorter (FACS). Cytogenetic, isoenzyme and DNA analysis confirmed the presence of human chromosome 12 in the CD4+ hybrids, and revealed that CD4 expression by TF42 was associated with multiple copies of this chromosome. Of seventy mAb recognizing human T-cell antigens screened on the CD4+ and CD4− variants of the two hybrids, only mAb recognizing CD4 and Leu 8 reacted with the CD4+ cells. These hybrids should be useful in the preparation, screening and analysis of anti-CD4 monoclonal antibodies, and in studies of CD4 epitopes recognized by HIV.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cancer immunology immunotherapy 16 (1983), S. 117-122 
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We describe an acute myelomonocytic leukaemia (E72) devoid of cell-surface HLA-DR antigens, but capable of inducing cellular responses. Leukaemia E72 induced proliferation of normal lymphocytes in primary mixed lymphocyte culture (MLC), which was only weakly inhibited by anti-DR sera. Depletion of a small percentage (≃4%) of DR+ cells on a cell-sorter failed to abrogate the capacity of E72 to stimulate MLC and cell-mediated cytotoxicity (CMC) responses. We found that normal lymphocytes primed with E72 responded in secondary MLC to lymphocytes and leukaemias, suggesting that the lymphocyte-activating determinant (LAD) on E72 is not leukaemia-specific. In addition, E72 induced CMC responses to both leukaemias and lymphocytes. We suggest that E72 may express a novel HLA or non-HLA LAD.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Cancer immunology immunotherapy 15 (1983), S. 39-46 
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Allogeneic lymphocytes can stimulate cell-mediated cytotoxicity (CMC) in lymphocytes from leukaemia patients against autologous leukaemia target cells. We have compared the capacity of different allogeneic lymphoid cells to stimulate CMC to fresh (i.e., patient) and cultured (MOLT 4, K562) leukaemic target cells in lymphocytes from an acute leukaemic patient and his HLA-identical siblings. Allogeneic lymphoid cells, and particularly a lymphoblastoid cell line, were effective in stimulating CMC to leukaemia targets. In some instances, however, leukaemia cells derived from the patient, mixed with allogeneic lymphoid cells stimulated synergistic CMC to the patient's leukaemia. We also found that the patient's leukaemia cells alone were able to stimulate CMC in HLA-identical sib lymphocytes to fresh and cultured leukaemia targets. Extra specificities on fresh leukaemia cells were revealed when these cells induced unpredicted CMC on normal lymphocyte targets when added to mixed lymphocyte cultures (MLC) between related and unrelated lymphocytes. Cytotoxic lymphocytes generated in MLC against the patient's HLA antigens were absorbed by monolayers of lymphocytes and leukaemia cells of the same HLA type as the patient, leaving residual CMC to fresh (patient) and cultured (K562) leukaemia target cells. In addition, CMC to the patient's leukaemia cells, stimulated in lymphocytes from the patient's HLA-identical sib by allogeneic cells, was absorbed by a monolayer of these allogeneic cells. This suggests cross reactivity between determinants on the leukaemia and allogeneic lymphocytes. The results of this study are consistent with expression of ‘leukamia antigens’, which are not restricted to leukaemia cells but may also be expressed on lymphocytes.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cancer immunology immunotherapy 13 (1982), S. 56-61 
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty-two human leukaemias, comprising acute phase leucocytes from 13 acute myeloid and nine lymphoid leukaemias, were tested for susceptibility to spontaneous cell-mediated cytotoxicity (CMC) by untreated lymphocytes and lymphocytes treated for 18 h with 250 IU lymphoblastoid (Namalva) interferon (IFN-α). IFN-amplified killing (IAK) by lymphocytes from 24 normal lymphocyte donors was checked on the K562 erythroleukaemia cell line, for comparison with IAK on fresh leukaemias. Nine leukaemias were tested with lymphocytes from three donors, nine with lymphocytes from six donors, three with lymphocytes from nine donors, and one with lymphocytes from 11 donors. Some degree of susceptibility to IAK was found in five acute myeloid and five lymphoid leukaemias, which was markedly dependent upon the source of the effector lymphocytes and did not correlate with the degree of IAK on K562. The 12 other leukaemias were virtually resistant to IAK. The results emphasize the variability in the capacity of IFN-treated lymphocytes to lyse leukaemias that have not been adapted to tissue culture. The basis of effector recognition of cell line and fresh tumour targets is discussed.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] We report that ICV administration of GLP-1 reduces food intake in fasted rats, with greater effect at higher doses (Fig. Ib). ICV injection of GLP-1 in rats at the beginning of the dark (feeding) phase also results in a profound decrease in feeding (Fig. la). When administered intraperitoneally up ...
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Cancer immunology immunotherapy 5 (1979), S. 263-274 
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tests comparing lymphocytes from normal controls, remission AML patients not receiving immunotherapy, and AML immunotherapy patients showed that cell-mediated cytotoxicity (CMC) to allogeneic AML cells requires in vivo priming and in vitro stimulation by AML cells. An in vitro lymphoproliferative response to allogeneic AML cells correlated with the development of CMC in immunotherapy-primed lymphocytes, though proliferation did not always lead to CMC. This may be due to differences in the lytic susceptibility of different AML cells. AML-stimulated CMC was cross-reactive on normal allogeneic PHA-transformed lymphoblasts and on lymphoblastoid cell lines (LCL). There was extensive cross-reactivity on allogeneic AML targets not used as in vitro stimulators. However, LCL generally did not induce CMC to allogeneic AML cells. CMC was generally absent, except in a few tests, on autologous PHA-transformed lymphoblasts following in vitro stimulation with allogeneic AML cells. CMC on autologous AML cells was equivocal, with little evidence for cross-reactive tumour-associated antigens in AML. Whilst CMC in this system was correlated with in vivo priming by immunotherapy, it is unlikely that such restimulated lymphocytes are the mediators of host-leukaemic cell cytolysis in vivo.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary It is not clear whether Down syndrome, the phenotypic expression of constitutional trisomy for chromosome 21 (T21), is the result of generalised disruption of homeostasis resulting from genetic imbalance, or the over-expression of specific genes on chromosome 21. In order to understand the effect of gene dosage more clearly, we have analysed the predicted and actual levels of expression of the leucocyte integrin β subunit CD 18 on the surface of T21 leucocytes. Previous studies showed that CD 18 expression by T21 lymphoid cell lines (LCL) is greater than on normal LCL. We have now developed a computer model that compares the observed and predicted CD 18 flow cytometric profiles for trisomy 21 LCL. Three parameters (α, β and γ) have been defined that measure different aspects of gene dosage. Using the computer model to calculate these parameters, we have carried out a series of paired comparisons between normal and T21 LCL. The results show that, in some T21 LCL, increased CD 18 expression is proportional to the existing gene dosage, in another set the effect is additive, whereas in others there is a combination of proportional and additive effects. The results suggest that gene regulation can exert pleiotropic effects on gene-dosage, and is consistent with a model in which gene dosage itself is the cause of disrupted homeostasis.
    Type of Medium: Electronic Resource
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