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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 7 (1980), S. 0 
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Mouse strains differ widely in their natural killer(NK)-cell activity. In the (A X B6) X A backcross, high reactivity was linked to H-2b, although non-H-2-linked genes were also demonstrated (Petranyi et al., 1975). Harmon et al. (1977) demonstrated an H-2Dd-associated reactivity gene (1977). In the present study, we have tested eleven B10 congenic strains for NK activity. The H-2Dd strains B10.A, B10.T(6R), B10.S(7R), B10.HTT and B10.D2 were more highly reactive than B10, B10.S, B10.G, B10.A(2R) and B10.BR, which do not carry the d allele at the H-2D locus. While this confirms the H-2Dd association of a reactivity gene, an exception was found in the B10.A(5R) strain that was low reactive in spite of the fact that it carries H-2Dd. This suggests the possibility that the H-2Dd-associated gene is outside H-2, to the right of Tla.The AKR.H-2b congenic line had the same low activity as the AKR.H-2k strain; both were much lower than B6. This suggests either one of two possibilities: the H-2b-linked reactivity gene is relatively distant from the H-2 complex, although localized on chromosome 17 or alternatively, if localized within or in the close neighbourhood of H-2, it requires non-H-2 genes for full expression.Previously, we have shown that the B6 X DBA/2 F1 hybrid was more highly reactive than either one of its two parental strains (Klein et al., 1978). A similar complementation effect is described in the present paper for the B10.D2 congenic strain. The high reactivity of this line can be due to the combined effect of an H-2b-linked gene from DBA/2 and the non-H-2 background of B10 or, alternatively, the former, together with an H-2b-linked gene from B6 that lies well outside outside the H-2 locus itself.
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 13 (1986), S. 0 
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The RBL-5 lymphoma has previously been shown to be highly sensitive to natural hybrid resistance, under the control of H-2 genes at the host level. The present study of the RBL-5 tumour was focused on progression towards disseminated growth after intravenous (i.v.) inoculation in the syngeneic host and the possible influence of the MHC genes at the tumour cell level. Data are presented to illustrate that there is no obligatory association between reduced H-2 expression and increased malignancy, and that the opposite may be observed. The wild type RBL-5 line expressed readily detectable H-2K and H-2D products, and a highly malignant subline selected for lung colonization in vivo did not show any reduction but rather enhanced expression of these antigens. Depending on the inoculum size, this selected subline caused disseminated lymphoma (in the liver, spleen and lungs) at a faster rate or higher frequency of animals than the wild type line. Conversely, a subline selected for reduced H-2 expression in vitro, by repeated treatments with antibody and complement, failed to form colonies in any organ after i.v. inoculation, even if the cell dose was increased by more than 100-fold in comparison with the threshold dose for the wild type tine. This H-2-deficient subline was completely resistant to syngeneic RBL-5 immune cytotoxic T lymphocytes (CTL). Clones isolated during selection of the subline showed different degrees of reduction in sensitivity to H-2 specific CTL, but an inverse pattern of sensitivity to poly I: C induced natural killer (NK) cells. Selection pressure imposed by NK-mediated elimination directed preferentially against cells with reduced H-2 expression may be one explanation of why the gain of histocompatibility antigens is associated with tumour progression in some systems. Another important implication taken up for discussion is that tests for the effect of MHC modulation on tumour growth or immunotherapy require careful experimental design, to cover the action of different effector mechanisms in viva
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