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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Immunogenetics 22 (1985), S. 543-552 
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Immunity against PCC3 teratocarcinoma cells (129, H-2 b) was induced in allogeneic (C3H, H-2 k) mice by preimmunization with L cells (C3H, H-2 k) expressing cosmid-introduced K b or D b genes, but not with nontransfected L cells. In addition, the growth of PCC3 cells in sublethally irradiated (C3H × B6-H-2 bm1)F1 and (C3H × B6-H-2 bm13 )F1 mice bearing the K bm1 and D bm13 mutations, respectively, was either prevented, stopped, or delayed in comparison with the (C3H × B6)F1 (k × b) mice, which failed to reject the PCC3 cells. The teratocarcinoma line OC15S was exceptional because it reacted specifically with Kb- and Db-specific (but not Ib-specific) alloantisera, and because Kb- and Db-specific antibodies could be absorbed by OC15S cells. The subpopulation of OC15S cells bearing the ECMA-7 antigen characteristic for embryonic carcinoma (EC) cells was isolated by the fluorescence-activated cell sorter and was shown to react specifically with Kb- and Db-specific antisera. These experiments show that teratocarcinoma cells express antigens similar or identical to the K-and D-region products of differentiated cells. The lack of expression of class I antigens is thus neither a condition nor a consequence of the pluripotentiality of the EC cells. The exact nature of the major histocompatibility complex antigens on EC cells has yet to be established using the methods of molecular biology and biochemistry.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Immunogenetics 24 (1986), S. 416-422 
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract While the role of the H-2 complex in the resistance to virally induced tumors has been extensively studied, little is known about its influence on the development of epithelial tumors of non-viral etiology, although such tumors are most prevalent in humans. Therefore, we analyzed the role of the H-2 complex in susceptibility to mammary tumors induced by hormonal stimulation from heterotopic hypophyseal isografts in H-2 congenic strains from C57BL/10, BALB/c, and 020/A backgrounds. This method of induction allows an assessment of the effect ofH-2 genes on the function of various organs involved in this process. We found that the tumor susceptibility genes map to two segments: PE-S, and to the right of S. The mechanisms by which the H-2 complex affects the induction of mammary tumors in C57BL/10 congenic strains seem to include an influence on several factors involved in the hormonal stimulation, because the susceptible B10 congenic strains have higher plasma levels of prolactin and the H-2 complex also affects the growth of hypophyseal isografts. Their size correlates with tumor development in individual mice in the resistant C57BL/10 congenic strains. We reported previously H-2-dependent differences in levels of the estrogen receptor in hypophysis. For this study, we measured the levels of estrogen receptors in uteri to assess the tissue specificity of this effect of H-2. However, no influence of the H-2 complex on estrogen receptor levels was observed in uteri. Strains from BALB/c and 020 backgrounds developed mammary tumors much earlier than the B10 congenic strains, indicating a strong influence of non-H-2 genes.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Immunogenetics 15 (1982), S. 477-484 
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In capping experiments with peripheral T lymphocytes, two anti-H-2.28 sera (AKR anti-AKR.L, anti-Kb, and C3H anti-0H.B10, k anti-b) that do not contain any Qa-2-specific antibodies are able to redistribute not only the H-2.28-positive H-2 molecules, but also Qa-2 molecules. This is due to the capacity of these sera to react with Qa-2 molecules because on cells where all known molecules of the H-2 d haplotype were capped (K1d, K2d, Dd, Md, Ld, L2d), both antisera still reacted when the cells came from a Qa-2 positive Dd strain (B10.A) but not when the cells were of Qa-2 negative strain (BALB/cByA). The reaction with la and non-H-2 antigens was excluded in these experiments. These data show that Qa-2 and H-2 antigens share some specificities of the H-2.28 family. Other anti-private and anti-public anti-H-2 sera failed to react with the Qa-2 molecules.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Immunogenetics 22 (1985), S. 183-188 
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In tests with 72 human donors, the outcome of the xenogeneic human-mouse MLR was influenced more by the general capacity of the human responder cells to react than by the MHS genotype of the mouse stimulating cells. While the response of the human lymphocytes of the same donor to the lymphocytes of six congenic mouse strains with differentH-2 haplotypes was generally rather similar, there were pronounced differences among individual human donors in the reactivity in these tests. These differences correlated with HLA, since the low reactivity was associated with the presence of the antigens HLA-AW25, HLA-B18, and HLA-DW2. The effect of the presence of antigens AW25, B18 was much more pronounced in males than in females. The low capacity to react in xenogeneic MLR in individuals with antigens HLA-AW25 and HLA-B18 may be the result of the general immune insufficiency associated with these antigens, which also includes C2 defficiency and association with immunopathological diorders.
    Type of Medium: Electronic Resource
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  • 7
    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
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 16 (1989), S. 0 
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Investigation of the antigenic phenotype of activated lymphocytes using the broadly cross-reactive mAb 6.3.4 revealed two phenotypic alterations as compared with the resting lymphocytes. The Qa specificity Qa-m208 disappears after lectin activation of Qa-m208-positive T lymphocytes. Analysis of Q7 and Q9 transfectants expressing the Qa-2 polypeptides shows that Qa-m208 is an epitope of the Qa-2 antigen. Because the Qa-2 antigens are still expressed on T lymphoblasts which have lost Qa-m208, changes of the Qa-2 molecules occur and result in the loss of certain epitopes.The second phenotypic change that we observed is the appearance of a novel specificity, Qa-12. Its expression is induced by lymphocyte activation and it is expressed on lymphoblasts of both T and B cell origin. The presence of this novel non-ubiquitous antigenic specificity is determined by the Tla region.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Serological and genetic analyses of H-2 antigens indicate that each K or D region allele controls two highly polymorphic antigenic sites, the alpha site corresponding to the private specificity and the gamma site corresponding to the long public specificities. Studies of cell surface distribution and biochemical characteristics of the alpha type specificity H-2.4 and gamma type specificity H-2.28 in the product of a D region allele, Dd, demonstrate that these specificities are carried on two different polypeptide chains. Accordingly, two distinct and polymorphic genes are postulated to code for the product controlled by the D region of H-2.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 2 (1975), S. 0 
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: It is well known that the major histocompatibility system (MHS) has unique properties pertaining to antigenic strength (Démant, 1973). In the 1973 and 1975 Workshops we investigated alloimmune interactions to try to find out which MHS genes are involved and how they confer antigenic strength. We found that in several models there are special antigenic strength conferring and/or controlling genes, that there are probably several such genes unique for each model, situated throughout the mouse MHS (H-2 complex). For example, the cell mediated lympholysis (CML) controlling genes, the Effector Cell Stimulating (ECS) genes, conferring strength against K and D region antigens are in the I region but separate from the I-A Lad genes (Festenstein et al., 1974) while the allograft controlling genes, for various rejection models, are in the D region as well as the I region (Festenstein et al., 1975). This is an attempt to bring together the data from these various models to formulate a functional concept of antigenic strength, in relation to its genetic basis.
    Type of Medium: Electronic Resource
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