Two allelic forms of mouse beta 2-microglobulin.

Robinson, Peter; Graf, Lynn; Sege, Karin

doi:10.1073/pnas.78.2.1167

Cited by 32 publications

(9 citation statements)

References 14 publications

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“…Thus, taken together the data from Tables 1, 2, and 3 strongly suggest that we can assign mouse B2m to mouse chromosome 2. To confirm this assignment, we analyzed the chromosome constitution of nine informative hybrid clones, including the two clones discordant for B2M and the chromosome 2 enzyme marker AK-1. The karyotype analyses revealed that chromosome 2 was the only mouse chromosome consistently concordant with mouse B2M in these hybrids ( Our results are consistent with the recent observation that the distribution of B2M isotypes in a series of recombinant inbred mouse strains follows that of Ly-4 and H-3, which are cell surface antigens encoded by genes on mouse chromosome 2 (6,12). Although it has been suggested that B2M, Ly-4, and H-3 are identical (6), we believe that this is unlikely because Ly-4 antigen is restricted to lymphocytes whereas B2M is expressed on most nucleated cells (29).…”

supporting

confidence: 79%

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Assignment of the gene for beta 2-microglobulin (B2m) to mouse chromosome 2.

Cox¹,

Sawicki²,

Yee³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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We have assigned the gene (B2m) coding for murine P2-microglobulin (B2M) to mouse chromosome 2 by using a novel panel ofChinese hamster-mouse somatic cell hybrid clones. Because the 35 independent primary hybrids used in this study were derived from two types of feral mice, each with a different combination of Robertsonian translocation chromosomes, as well as from mice with a normal complement of acrocentric chromosomes, analysis of 16 selected mouse enzyme markers provided data on the segregation of all 20 mouse chromosomes in these hybrids. Mouse B2M was identified in cell hybrids by immunoprecipitation with a species-specific anti-mouse B2M antiserum followed by two-dimensional polyacrylamide gel electrophoresis of the immunoprecipitated polypeptides. Enzyme analysis ofthe segregant clones excluded all chromosomes for B2m assignment except mouse chromosome 2, and karyotype analysis of nine informative hybrid clones confirmed the assignment of B2m to this chromosome. These results demonstrate that, in the mouse, as in man, B2m is not linked to the major histocompatibility or immunoglobulin loci.

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supporting

confidence: 79%

“…The chromosomal location of the gene coding for B2M in other species is not known. Recently, allelic forms of B2M in the mouse have been described, and preliminary studies have suggested linkage between B2m and genes coding for the Ly-4 and H-3 antigens, which have been assigned to mouse chromosome 2 (11,6,12).…”

mentioning

confidence: 99%

Assignment of the gene for beta 2-microglobulin (B2m) to mouse chromosome 2.

Cox¹,

Sawicki²,

Yee³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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“…Recombinant mouse IFN-y was kindly provided by Dr. Svetly (Boehringer, Vienna, Austria). [34]; rabbit anti-rnouse-fl2m serum, recognizing the free P2m protein [35]; 17/227: anti-1-Ab [36]. F ( a b ' )~ fragments of the mAb 28-8-6s were produced according to the method of Parham [37] and Lamoyi and Nisonoff [38]: 2 mg/ml of antibody was digested with 45 pg/ml of pepsin for 8-9 h at 37°C.…”

Section: Cell Lines and Mediamentioning

confidence: 99%

Reconstitution of H‐2 class I expression by gene transfection decreases susceptibility to natural killer cells of an EL4 class I loss variant

Sturmhöfel

Hämmerling

1990

Eur J Immunol

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Several reports have suggested that an inverse correlation exists between major histocompatibility complex class I expression and the susceptibility to natural killer (NK)-mediated lysis. For example, the increased class I expression induced by interferon-gamma was always accompanied by an increased resistance to NK lysis. Likewise, class I loss variants were often more NK susceptible than their normal counterparts. To investigate whether the inverse correlation between class I expression and NK susceptibility was fortuitous or whether the class I molecules were directly responsible for this effect we resorted to gene transfection studies. From the murine thymoma line EL4 and H-2Db- and Kb-negative variant S3 was selected. This variant was highly susceptible to NK lysis. S3 was found to have a defect in beta 2-microglobulin gene expression. Therefore, restoration of Db and Kb expression could be achieved by transfection with the beta 2-microglobulin gene. This resulted in a strong decrease in susceptibility to NK lysis to the level of the H-2+ parental EL4. Transfection with class II genes had no effect. Blocking of the class I molecules on the H-2+ cells with anti-H-2b F(ab')2 fragments increased the susceptibility to NK cells to the level of the H-2- variant S3. These data demonstrate that the class I molecules on the targets are directly responsible for regulation of NK susceptibility but the mechanism is not clear. Possibly the class I molecules interfere with the unknown NK target structures.

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“…The allelic form of /?2-microglobulin &m), a genetic marker which can distinguish between mice of the B10 and those of BALB/c background (Michaelson, 1980;Robinson et al, 1981), was evaluated in YC8 cells by immunochemical methods. Rabbit anti-mouse P2-m and rabbit anti-H-2a sera were kindly provided by Dr. M.J. Rogers (N.I.H., Bethesda, MD, USA) and used to precipitate NP40-solubilized, Lens culinaris affinity-chromatography-purified and lUIlabelled H-2 antigens of YC8 cells.…”

Section: Analysis Of the Allelic Forms Of Isozymes And Pz-microglobulinmentioning

confidence: 99%

Cross‐reactions between tumor cells and allogeneic normal tissues. inhibition of a syngeneic lymphoma outgrowth in h‐2 and non‐h‐2 alloimmune balb/c mice

Parmiani

Sensi

Carbone

et al. 1982

Intl Journal of Cancer

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To test whether alloimmunization with H-2 or/and non-H-2 different normal tissues may increase the immunity to syngeneic tumors, groups of BALB/c (H-2d) mice were immunized with a series of allogeneic lymphoid cells and then challenged i.p. with syngeneic lymphoma cells. The outgrowth of otherwise lethal doses of the Moloney virus-induced lymphoma YC8 and of its clones was inhibited in BALB/c mice immune to DBA/2 (H-2d), C3Hf (H-2k), C3H.SW (H-2b), C3H.OH (H-2o2) and to B10 background tissues but not in mice immunized to A/He, BALB.K (H-2k) or BALB.B (H-2b) normal tissues. Anti-YC8 effect was also induced by immunizing BALB/c recipients with a pool of five different allogeneic cell lines which included C3Hf, C57BL/6J (H-2b), N:NIH (H-2q), B10.M (H-2f), and DBA/2 lymphoid cells. No growth inhibition of other BALB/c lymphomas induced by Moloney virus (LSTRA), X-rays (RL male I) or urethane (UR-1) was evident in alloimmune mice. In vivo transfer of growth inhibition of YC8 was obtained with BALB/c anti-B10.D2 peritoneal exudate cells in a Winn assay. The ability of these alloimmune lymphoid cells to delay significantly the survival time of BALB/c mice injected with the mixture of immune cell and YC8 cells was abrogated by anti-Thy 1.2 plus C' treatment. In addition, nu/nu BALB/c mice were unable to develop resistance to YC8 outgrowth after alloimmunization. The results of this study show that: (1) syngeneic growth of a lymphoma can be prevented by alloimmunization with normal cells; (2) this cross-reaction involved non-H-2 antigens; (3) the phenomenon appeared to be mediated by T cells.

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Two allelic forms of mouse beta 2-microglobulin.

Abstract: Two allelic forms of mouse 32-microglobulin (,2m) Preliminary structural studies indicate differences in peptide composition between the two forms.

Cited by 32 publications

References 14 publications

Assignment of the gene for beta 2-microglobulin (B2m) to mouse chromosome 2.

Assignment of the gene for beta 2-microglobulin (B2m) to mouse chromosome 2.

Reconstitution of H‐2 class I expression by gene transfection decreases susceptibility to natural killer cells of an EL4 class I loss variant

Cross‐reactions between tumor cells and allogeneic normal tissues. inhibition of a syngeneic lymphoma outgrowth in h‐2 and non‐h‐2 alloimmune balb/c mice

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