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Biomedical subjects

J Klein

Publications and source records attributed to J Klein.

At least 919 records · Page 51Linked to original sources
PubMed1976

Ability of H-2 regions to induce graft-vs-host disease.

Individual young adult F1 hybrid mice were irradiated with 500 R and 24 hr later injected with 5 X 10(7) spleen cells obtained from a sex-matched parental-strain donor. The injected animals were then followed for a period of 3 months and loss of body weight, mortality rate, and other signs of fatal graft-vs-host disease (GVHD) were recorded. The donor-recipient strain combinations were selected in such a way as to provide genetic differences in the entire H-2 complex, the K or D regions alone, the K or the D end, and the central (I) regions alone. The data obtained on only few combinations indicate that strong GVHD (100% mortality rate within the first month after the injection) occurs only in those donor-recipient combinations which differ in the entire H-2 complex or in the K end (K + I regions). Much weaker GVHD (mortality rate of only 50% or less and death of individual mice spread over the entire observation period) is observed when the donor and the host differ in either the K, I, or D region alone. The degree of GVHD induced by three regions, when taken singularly, is about the same. Surprisingly, the K-region GVHD was somewhat stronger in combinations of mutant strains in comparison with recombinant-strain combinations.

Animals↗
PubMed1975

Linkage disequilibrium between H-2 and t complexes in chromosome 17 of the mouse.

Mice with t factors belonging to the same complementation group carry similar, if not identical, H--2 haplotypes although these factors were derived from widely separated geographical areas. This association between t and H--2 complexes suggests more than a casual relationship between the two complexes, at least at the population level.

Animals↗
PubMed1975

Studies on the murine Ss protein. I. Purification, molecular weight, and subunit structure.

The murine Ss protein has been isolated and purified. Using specific antisera, the radiolabeled protein has a mol wt of 120,000 in sodium dodecyl sulfate polyacrylamide gels. It is composed of two basic subunits of 23,000 and 14,000 daltons. The smaller molecular weight subunit contains a single disulfide bridge, is devoid of carbohydrate, and may represent the murine equivalent of beta2-microglobulin.

Amino Acid Sequence↗
PubMed1975

Molecular relationship between private and public H-2 antigens as determined by antigen redistribution method.

Molecular relationship of public H-2 antigens 1, 5, 6, 8, 11, 13, 25, and 28 to private antigens controlled by K and D regions was studied using the technique of antibody-induced resistance to complement-mediated cytotoxicity. The results indicate physical association in the cell membrane between H-2 antigens 1 and 23 of H-2-a, 8 and 31 of H-2-d, 11 and 17 of H-2-q, 13 and 30 of H-2-q, 25 and 23 of H-2-k, and 28 and 31 of H-2-g. These results are in agreement with genetic mapping placing the determinants of antigens H-2.8, 11 and 25 in the K region , the determinant of antigen H-2.13 in the D region, and the determinants of antigens H-2.1 and 28 in either the K or the D region. In contrast to genetic mapping placing the determinant for antigen H-2.6 in the D region, we found that in the H-2-b haplotype the antigen is associated with K region antigen H-2.33 and H-2.32, and interpreted this result as evidence for two homologous H-2.5 sites controlled by opposite ends of the H-2 complex. Although the data do not prove that public antigens are carried by the same molecules as private ones, they demonstrate a close physical association in the membrane between the two groups of loci, K and D, coding for the first 33 classical H-2 antigens (with the exception of antigen H-2.7), and thus support the two-locus model. The data also support the duplication model of H-2 by demonstrating two homologous H-2.5 sites associated with K and D molecules.

Animals↗
PubMed1975

Induction of resistance to antibody-mediated cytotoxicity. H-2, Ia, and Ig antigens are independent entities in the membrane of mouse lymphocytes.

Mouse spleen or thymus lymphocytes incubated with monospecific H-2 or Ia alloantisera and then coated with a xenogeneic antimouse Ig serum become specifically resistant to the alloantiserum (and complement) they have been incubated with. This so called "lysostrip method" was used to investigate the molecular interrelationships of antigens in the mouse lymphocyte membrane. The results of this investigation confirm that H-2K and H-2D antigens are carried by two distinct populations of molecules. They provide evidence that the Ia antigens move in the membrane independently of both H2-K and H-2D antigens; and finally they demonstrate absence of any physical linkage between Ig receptors in B cells, on the one hand, and Ia, H-2K, and H-2D molecules on the other hand.

Animals↗
PubMed1975

A method for detection of Ia antigens in the absence of appropriate H-2 recombinants.

A method is described which obviates the use of H-2 recombinant strains for production and detection of Ia antibodies. The antibodies are produced by immunization with spleen cells in a strain combination in which the donor differs from the recipient either in the K end of the H-2 complex or in the whole complex. If the right schedule is used, this immunization produces antibodies against both H-2 and Ia antigens. The H-2 antibodies are absorbed out with erythrocytes or T lymphocytes rendering the antiserum specific for Ia antigens. The presence of Ia Ia antibodies is asserted by determining the tissue distribution of the antigens detected with the absorbed antiserum. Another antiserum is then prepared in the same strain combination by immunization with tissue that does not contain Ia but does contain H-2 antigens (e.g., a sarcoma of the proper genotype). The second antiserum contains only H-2 antibodies and the presence of these antibodies is again asserted by determining the tissue distribution of the corresponding antigens. The molecular distinctiveness of the putative Ia and H-2 antigens is then demonstrated by the newly developed technique of antibody-mediated induction of resistance to cytotoxicity (lysis). If the antigens detected with the two antisera move independently in the cell membrane, and if the antigens detected with the first antiserum do indeed have Ia-like properties, it is concluded that the antiserum detects Ia antigens. This method should prove to be useful for detection of Ia antigens in H-2 haplotypes for which no intra-H-2 recombinants are known, and for detection of Ia-like antigens in other mammalian species, particularly in man.

Absorption↗
PubMed1975

Immunogeneic analysis of H-2 mutations. II. Cellular immunity to the H-2DA mutation.

The H-2da haplotype was derived from the H-2d haplotype by a mutation localized to the D end of the H-2 complex. Coculture of H-2d and H-2da spleen cells gives rise to bidirectional MLR. However, the H-2d anti-H-2da response is much stronger than that of H-2da anti-H-2d. Both haplotypes give rise to reciprocal CML. B10.D2(R103) strain spleen cells, which differ only at the D end of the H-2 complex from the H-2d haplotype, kill H-2da target cells in CML when sensitized to H-2d stimulators and vice versa. Therefore, both the mutant and strain of origin share a D end CML specificity. H-2d and H-2da reject skin grafts in both directions, although some H-2d grafts show prolonged acceptance on H-2da recipients. These data are consistent with a mutation in the D end of the H-2d haplotype resulting in gain-loss of an antigen(s) that gives rise to reciprocal MLR, CML, and skin graft rejection. Further, the mutant can be distinguished from the strain of origin on the basis of the strength of immune response in MLR.

Animals↗
PubMed1975

Immunogenetic analysis of H-2 mutations. III. Genetic mapping and involvement in immune reactions of the H-2ka mutation.

Mutation M523 (H-2ka) occurred spontaneously in strain CBA/CaLacSto and was discovered during routine skin graft testing for genetic homogeneity. By linkage and complementation tests, the mutation was previously mapped in the K end of the H-2 complex. We demonstrate that the mutation occurred in the K region, without affecting the I region in the K end of the complex. The mutant antigens cause rejection of skin grafts, stimulate cells in mixed lymphocyte culture, and function as stimulators as well as targets in cell-mediated lymphocytotoxicity. Yet, they are serologically indistinguishable from the antigens of the original strain and do not induce formation of humoral antibodies upon immunization of the CBA strain. Together with the results obtained on testing of other H-2 mutants, the data strongly support the notion that classical H-2 antigens (i.e., products of the H-2K and H-2D loci) can function as lymphocyte-stimulating determinants, and that I-region differences are not required for the induction of strong cell-mediated lymphocytotoxicity.

Animals↗
PubMed1974

Serological distinction of mutants B6.CH(zl) and B6.M505 from strain C57BL-6.

A quantitative serological difference was found between strains Hz1 and M505 carrying mutant H-2 haplotypes ba and bd, respectively, and the original strain B6(H-2(b)). The finding suggests that the mutations occurred in the H-2K(b) gene, and together with data on MLR and CML challenges the current concept of H-2 regions' involvement in immune reactions.

Animals↗