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J H Stimpfling

Publications and source records attributed to J H Stimpfling.

At least 19 recordsLinked to original sources
PubMed1993

Meiotic recombination within the H-2K-H-2D interval: characterization of a panel of congenic mice, including 12 new strains, using DNA markers.

Intra-H-2 recombinant congenic strains are widely used to localize traits to specific subregions of the major histocompatibility complex and have provided evidence for the existence of meiotic recombinational hotspots in mammals. Forty-seven intra-H-2 recombinant strains, including 12 not previously reported, have been identified by serological typing in our laboratory. We have extended the analysis of the crossover sites in these mice using DNA markers for Ab, Aa, Eb, Ea, Cyp21-ps, D17Tu3, Bat7, and Bat5. The recombinant chromosomes of these congenic strains include loci derived from the a, b, f, k, p, q, r, s, u, and v haplotypes of H-2, providing a diverse panel of strains. Although some alleles of Bat7 could not be distinguished from one another, results from the majority of strains indicated a probable gene order of C4Slp/D17Tu3-Bat7-Bat5-H-2D. No recombinants between Cyp21-ps, C4Slp, and D17Tu3 were observed. The crossover sites in 31 of the 47 intra-H-2 recombinants were within the C4Slp/D17Tu3-H-2D interval; of these 31 crossovers, three were bracketed by D17Tu3 and Bat7, ten by Bat7 and Bat5, seven by Bat5 and H-2D, and 11 by D17Tu3 and Bat5. The results from all 47 strains suggest recombinational hotspots within the C4Slp/D17Tu3-H-2D interval and emphasize the influence that specific haplotypes can have on preferred crossover sites.

Animals↗
PubMed1992

Transplantation effects of a unique major histocompatibility complex class I mutation.

This study describes a novel MHC class I mouse mutant that was discovered because of loss of reactivity of its cells to monoclonal antibodies. The mutation occurred in the H-2Ks molecule and is the first in vivo mutation described that has a single altered amino acid residue (amino acid 107) distant from the regions considered to be peptide or TCR contacts. Nevertheless, skin grafts from the mutant to the parent are rejected by CD8+ T-cells. In the reciprocal direction, the mutant shows partial tolerance to parental skin grafts, suggesting that the mutant is inefficient in selecting alloreactive T-cells specific for the wild-type Ks molecule.

Animals↗
PubMed1985

Greying with age in mice: relation to expression of murine leukemia viruses.

Some strains of C57BL/10 H-2-congenic mice were found to exhibit greying with age, whereas others did not. Two patterns of greying were observed, diffuse greying beginning at 4 to 6 months of age and patterned greying beginning at 4 to 6 weeks. Strains exhibiting either greying pattern expressed high levels of infectious ecotropic and mink cell focus-inducing murine leukemia viruses (MuLV) in tests of thymus and spleen and in cultures from skin or tail biopsies, whereas nongreying strains expressed little virus until late in life. Electron microscopy demonstrated large accumulations of MuLV in grey, but not in black areas, of skin from a mouse with patterned greying. Infectious MuLV was produced spontaneously by embryos of greying, but not of nongreying, mice and pups of nongreying strains fostered on greying mothers turned grey after 3 months. These results suggest that greying with age results from melanocyte dysfunction that occurs subsequent to pre- or early postnatal infection with MuLV.

Aging↗
PubMed1984

Relationship between a retroviral germ line reintegration and a new mutation at the ashen locus in B10.F mice. Retroviral integration and an ashen mutation.

In a litter of B10.F mice a single mouse was found with a "dilute-like" coat-color mutation. F2 matings were then carried out to establish sufficient numbers of mice carrying this mutation in a homozygous form. The coat-color mutation was found to be allelic to the ashen locus which is closely linked to the dilute locus on chromosome 9. Further analysis of the ashen mice showed they contained an additional ecotropic provirus integrated into their chromosomal DNA. This result initially suggested that retroviral integration was responsible for the mutation. However, backcross studies showed the mutation and provirus were genetically unlinked. The reintegrated provirus was molecularly cloned and transfection studies showed the virus was B tropic in host range. The restriction map of the cloned provirus was found to be similar to previously described B-tropic viruses. The results are discussed in view of the low probability of two rare and unlinked events occurring in a single mouse.

Alleles↗
PubMed1984

Control of the immune response to the EA-2.1 alloantigen of the mouse by the H-2 complex.

The immunization of selected congenic strains and hybrids with the Ea-2.1 cellular alloantigen of the mouse shows that the anti-Ea-2.1 immune response is regulated by a gene or genes associated with the H-2 gene complex. It was earlier demonstrated that H-2r and H-2b were, respectively, responder and nonresponder haplotypes. In this report it is shown that the haplotypes H-2d and H-2g2 are also responder haplotypes, while H-2a, H-2k, H-2m, H-2p, H-2q, H-2awl and H-2u are nonresponder haplotypes. The responder H-2g2 and nonresponder H-2awl haplotypes are recombinant configurations that map the Ea-2.1 regulator gene, or genes, within or adjacent to the I-A subregion of the H-2 gene complex.

Animals↗
PubMed1982

Antigen-specific soluble helper activity for murine major histocompatibility complex-encoded molecules. I. Kinetics of factor production after skin transplantation and genetic mapping of the H-2 region specificity.

Antigen-specific soluble helper molecules are produced during major histocompatibility complex-disparate allograft priming. Genetic mapping studies with appropriate recombinant and mutant lines of mice have defined the antigen specificities of the soluble helper molecules described here as being directed against the H-2Dd molecules. The production of antigen-specific helper molecules is a relatively early event after H-2Dd-region allograft priming. A later phase of factor production near the time of graft rejection also contains nonspecific helper factors and IL-2.

Animals↗
PubMed1979

Gene complementation in the T-lymphocyte proliferative response to poly (Glu55Lys36Phe9)n. A demonstration that both immune response gene products must be expressed in the same antigen-presenting cell.

The immune response (Ir) to the random copolymer GLphi depends upon the function of two Ir genes, Ir-GLphi-beta[beta] and Ir-GLphi-alpha[alpha], mapped to the I-A and I-E/C subregions of the major histocompatibility complex, respectively. In this paper, the site(s) of expression of the products of these two Ir genes was examined by evaluating T-lymphocyte proliferative responses of bone marrow radiation chimeras. Chimeras were created in [alpha+beta- X alpha-beta+]F1 responder mice by lethal irradiation and reconstitution with a mixture of bone marrow cells from both parental strains. These chimeras failed to respond to GLphi, although they were capable or responding to the much weaker antigens, (T,G)-A--L, TEPC-15, pigeon cytochrome c, and (H,G)-A--L. This failure to respond to GLphi was shown not to be the result of a cryptic mixed lymphocyte reaction, as similar chimeras created in (alpha+beta+ X alpha-beta+)F1 mice responded well to GLphi, although they possessed almost the same potential histoincompatibility. Furthermore, the lack of response to GLphi could not be attributed to a general failure of the two parental cell types in the chimeras to collaboratc with each other, as each chimeric parental cell type could respond to dinitrophenyl conjugated ovalbumin presented on nonimmune spleen cells from the other parent. Thus, the failure of low responder parental into F1 high responder chimeras to generate an immune response to GLphi suggests that immune competence for this antigen requires at least one cell type in the immune system to express gene products of both the Ir-glphi-alpha and -beta genes, i.e. one cell must be of high responder genotype. The the antigen-presenting cell is one such cell type was shown by experiments in which GLphi-primed T lymphocytes from responder F1 mice were stimulated with antigen bound to nonimmune spleen cells. Only spleen cells from responder F1 and recombinant mice could present GLphi. Neither of the two complementing nonresponder parental spleen cell populations, either alone or mixed together, could present GLphi, although both could present purified protein derivative of tuberculin. This was shown to be the case for T cells positively selected in vitro as well as freshly explanted T cells. Thus, both Ir-GLphi-alpha and Ir-GLphi-beta gene products must be expressed in the same antigen-presenting cell to generate a T-lymphocyte proliferative response to GLphi. The implications of these findings for models of two gene complementation are discussed.

Animals↗
PubMed1979

Gene dose effects in Ir gene-controlled systems.

(B10.A x B10.S)F1 hybrid mice produce lower levels of anti-GL phi antibody than B10.S(9R) and B10.HTT mice. To determine whether this difference is due to a gene dose or a cis-trans effect, [B10.S(9R) x B10.S(8R)]F1 mice were immunized with GL phi. These mice carry one dose of the responder Ir gene alleles in the cis position whereas the recombinant B10.S(9R) and B10.HTT mice carry two doses of the relevant genes. Both (B10.A x B10.S) and [B10.S(9R) x B10.S(8R)] F1 mice produced comparably lower amounts of antibodies as compared to the recombinant strains. The data therefore demonstrate that gene dose and not cis-trans effect accounts for the differences between F1 and recombinant strains in their antibody response to GL phi controlled by complementary Ir genes.

Animals↗
PubMed1977

Coupled complementation of immune response genes controlling responsiveness to the H-2.2 alloantigen.

The ability of various B10 congenic resistant strains to respond to the alloantigen H-2.2 was tested. High and low antibody-producing strains were distinguished by their anti-H-2.2 hemagglutinating respones. However, these strains do not differ in their ability to respond to these antigenic differences in the mixed lymphocyte culture. The humoral response to the H-2.2 alloantigen was shown to be controlled by two interacting genes localized within the H-2 complex. Thus, F1 hybrids prepared between parental low responder strains could yield high level immune responses. In addition, strains bearing recombinant H-2 haplotypes were used to map the two distinct genes controlling the immune response. The alleles at each locus were shown to be highly polymorphic as evidenced by the asymmetric complementation patterns observed. The restricted interactions of specific alleles was termed coupled complementation. The significance of the results in the terms of mechanisms of Ir gene control are discussed.

Alleles↗
PubMed1975

Characterization of immune response and mixed lymphocyte reactions in selected intra-H-2 recombinant strains.

The genes controlling the immune response to the random linear terpolymers GAT and GLpro have been mapped in the Ir-1A or Ir-1B subregions with five lines of H-2-s/H-2-a recombinant mice. The I region also contains a third subregion, I-C, which codes for a lymphocyte-activating determinant, Lad2, controlling mixed lymphocyte reactivity. The mixed lymphocyte responses associated with I-C region disparity are compared with the stimulation noted with other H-2 region differences. Unidirectional lymphocyte activitation was associated with the Lad2 determinants in selected combinations.

Animals↗
PubMed1973

Cell-mediated lympholysis. Importance of serologically defined H-2 regions.

The cell-mediated lympholytic capability of mouse spleen cells stimulated in mixed lymphocyte culture is related to the major histocompatibility complex genotype on target lymphocytes. The strain combinations AQR-B10. T(6R) and B10.A(4R)-B10.A(2R) that result in significant mixed lymphocyte culture activation do not mediate cell-mediated lympholysis on sensitizing target lymphocytes; serologically defined regions (H-2K and H-2D) are identical within each combination. H-2K or H-2D region disparity alone does not cause cell-mediated lympholysis. However after mixed lymphocyte culture activation as seen with B10.A-B10.T(6R), a target cell bearing only an H-2K region difference from the effector cell is sensitive to cell-mediated lympholysis. Likewise an H-2D region difference is an adequate target after mixed lymphocyte culture activation of the effector cell in the combination B10.A(2R)-B10.D2.

Animals↗