Natural resistance of lethally irradiated F1 hybrid mice to parental marrow grafts is a function of H-2/Hh-restricted effectors.

Daley, John P.; Nakamura, Ichiro

doi:10.1084/jem.159.4.1132

Cited by 45 publications

(18 citation statements)

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“…Intravenous injections of irradiated EL-4 cells, but not R1 cells, reduced the resistance. As previously shown, this indicates that the Hh-1 phenotype of the irradiated competing cells dictates whether the Hh-lb-positive B6 BMC grafts survive in the F 1 hosts (Daley and Nakamura 1984). Three independent clones of somatic cell hybrids between EL-4 and R1 cells were tested to determine their Hh-1 phenotype using the same assay.…”

Section: Resultsmentioning

confidence: 99%

“…Expression of Hh-1 b determinants on tumor cells was assessed by testing the irradiated cells' ability in vivo to block the rejection of parental B6 bone marrow cells (BMC) in lethally irradiated B6C3F 1 mice, as described (Daley and Nakamura 1984). Briefly, lethally irradiated (9.5Gy of-y rays) B6C3FÀ recipient mice were given intravenous (i. v.) injections of 5 x 107 tumor cells (irradiated at 100Gy) 24 h and 3 h before the i.v.…”

Section: Methodsmentioning

confidence: 99%

“…Tumor cells were labeled with [125I]-IUdR for 18 h as described (Daley and Nakamura 1984) and 106 cells in 0.5 ml of Hank's balanced salt solution (HBSS) were injected i. v. into each B6C3F~ mouse, which had been exposed to 9.5Gy of')' radiation. Three h after injection, spleens were removed and assessed for 12sI activity.…”

Section: Labeling Of Tumor Cells For Localization Studiesmentioning

confidence: 99%

“…However, in the absence of experimental evidence, other mechanisms, including posttranscriptional control, could provide an equally plausible explanation. For example, the requirement of homozygosity (Bennett 1972;Daley and Nakamura 1984) might reflect a need for two copies of the same allele for the expression of a threshold level of relevant determinants on the cell surface.…”

Section: Introductionmentioning

confidence: 99%

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Homopoietic histocompatibility (Hh-1) phenotype and the regulation of its expression

et al. 1992

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Hybrid resistance (HR) is primarily controlled by the genes of the Hemopoietic histocompatibility-1 (Hh-1) locus within the H-2 complex. HR is a consequence of the Hh-1-controlled target determinants in homozygous parental strain mice and their absence in heterozygous F1 hybrid mice. To examine the mechanism that controls the Hh-1 phenotype, three independent clones of somatic cell hybrids between parental lines EL-4 (C57BL/6 origin, H-2b) and R1 (C58 origin, H-2k) were studied. The line EL-4 is Hh-1b-positive and is subject to HR by H-2b heterozygous F1 mice, but R1 lacks the Hh-1b allele and is not susceptible to HR. Of the three hybrid clones, F263.2 is Hh-1b-positive, whereas the other two, F262.2 and F264.2, are Hh-1b-negative, as judged by these cells' capacity to compete in vivo with the grafted parental C57BL/6 bone marrow cells in the resistant (C57BL/6 x C3H)F1 mice. All three clones express the H-2b and H-2k class I antigens equally well, are susceptible to activated NK cells to the same extent, and all carry four copies of chromosome 17. However, Southern analysis reveals that clone F263.2 contains three copies of H-2b chromosome and one H-2k, whereas the other two clones carry two copies each of the parental chromosome 17. The results suggest that the relative copy number of specific alleles is the crucial determinant of the Hh-1 phenotype, and render unlikely both the gene dosage hypothesis and the trans-acting dominant suppression hypothesis to account for the noncodominant expression of the Hh-1 phenotype.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Labeling Of Tumor Cells For Localization Studiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Homopoietic histocompatibility (Hh-1) phenotype and the regulation of its expression

et al. 1992

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“…14 and 15). For example, H-2 b/k mice reject H-2 b marrow but accept H-2 k marrow (16). Therefore, we evaluated whether the frequency of H-2K k -negative T cells was different from the frequency of H-2K b -negative T cells in H-2 b/k mice.…”

Section: Nk-mediated Elimination Of Mutant Lymphocytes That Havementioning

confidence: 99%

NK-Mediated Elimination of Mutant Lymphocytes that Have Lost Expression of MHC Class I Molecules

Kusunoki

Kyoizumi

Honma

et al. 2000

The Journal of Immunology

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Mutant cells generated in vivo can be eliminated when mutated gene products are presented as altered MHC/peptide complexes and recognized by T cells. Diminished expression of MHC/peptide complexes enables mutant cells to escape recognition by T cells. In the present study, we tested the hypothesis that mutant lymphocytes lacking expression of MHC class I molecules are eliminated by autologous NK cells. In H-2b/k F1 mice, the frequency of H-2Kb-negative T cells was higher than that of H-2Kk-negative T cells. The frequency of H-2K-deficient T cells increased transiently after total body irradiation. During recovery from irradiation, H-2Kk-negative T cells disappeared more rapidly than H-2Kb-negative T cells. The disappearance of H-2K-deficient T cells was inhibited by administration of Ab against asialo-GM1. H-2Kk-negative T cells showed higher sensitivity to autologous NK cells in vitro than H-2Kb/k heterozygous or H-2Kb-negative T cells. Adding syngeneic NK cells to in vitro cultures prevented emergence of mutant cells lacking H-2Kk expression but had little effect on the emergence of mutant cells lacking H-2Kb expression. Results in the H-2b/k F1 strain correspond with the sensitivity of parental H-2-homozygous cells in models of marrow graft rejection. In H-2b/d F1 mice, there was no significant difference between the frequencies of H-2Kb-negative and H-2Kd-negative T cells, although the frequencies of mutant cells were different after radiation exposure among the strains examined. H-2b/d F1 mice also showed rapid disappearance of the mutant T cells after irradiation, and administration of Ab against asialo-GM1 inhibited the disappearance of H-2K-deficient T cells in H-2b/d F1 mice. Our results provide direct evidence that autologous NK cells eliminate mutant cell populations that have lost expression of self-MHC class I molecules.

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Class I H‐2D^b determinants are not involved in hybrid resistance to parental H‐2^b/Hh‐1^b bone marrow allograft

1987

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Hybrid resistance to parental H-2b bone marrow grafts is directed to a cell surface structure controlled by the Hh-1 locus in or near the H-2D region. The nature of this surface structure is not known. Since homozygosity at the class I H-2D locus or loci in this haplotype would seem a necessary but not sufficient condition for the grafts' susceptibility to resistance, we tested whether the expression of this phenotype is dependent on the expression of class I H-2Db determinants. Cloned variants of H-2b tumor RBL-5 were obtained by immunoselection for the absence of H-2Db expression, as determined by the inability to bind specific antibody and to induce or react with alloreactive cytotoxic T lymphocytes. The three clones used in this study were H-2Db negative but H-2Kb positive and were natural killer cell resistant. When tested in vivo as competitive inhibitors the variant cells were capable of blocking hybrid resistance to parental H-2b bone marrow grafts as were unselected H-2Db-positive parental line cells. Therefore, H-2Db expression is irrelevant for Hh-1b expression. An incidental observation was that YAC-1 cells, a non-H-2b tumor with pronounced susceptibility to natural killing, were able to block hybrid resistance. This reactivity, not observed in our previous studies, raises the possibility that at least some of the effector cells are cross-reactive or capable of dual recognition.

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Natural resistance of lethally irradiated F1 hybrid mice to parental marrow grafts is a function of H-2/Hh-restricted effectors.

Cited by 45 publications

References 29 publications

Homopoietic histocompatibility (Hh-1) phenotype and the regulation of its expression

Homopoietic histocompatibility (Hh-1) phenotype and the regulation of its expression

NK-Mediated Elimination of Mutant Lymphocytes that Have Lost Expression of MHC Class I Molecules

Class I H‐2D^b determinants are not involved in hybrid resistance to parental H‐2^b/Hh‐1^b bone marrow allograft

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Natural resistance of lethally irradiated F1 hybrid mice to parental marrow grafts is a function of H-2/Hh-restricted effectors.

Cited by 45 publications

References 29 publications

Homopoietic histocompatibility (Hh-1) phenotype and the regulation of its expression

Homopoietic histocompatibility (Hh-1) phenotype and the regulation of its expression

NK-Mediated Elimination of Mutant Lymphocytes that Have Lost Expression of MHC Class I Molecules

Class I H‐2Db determinants are not involved in hybrid resistance to parental H‐2b/Hh‐1b bone marrow allograft

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Class I H‐2D^b determinants are not involved in hybrid resistance to parental H‐2^b/Hh‐1^b bone marrow allograft