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Biomedical subjects

D W Bailey

Publications and source records attributed to D W Bailey.

At least 37 records · Page 2Linked to original sources
PubMed1980

Studies of two H-2Db mutants: B6. C-H-2bm13 and B6.C-H-2bm14.

Two new C57BL/6 H-2 mutants, B6.C-H-2bm13 and B6.C-H-2bm14 are described. They arose independently in C57BL/6 as spontaneous mutations of the gain and loss type. Complementation studies map the mutations in both bm13 and bm14 to the H-2Db gene. However, these two mutant strains are not identical, but occurred as independent mutations at the same locus, as shown by reciprocal graft rejection and by the inability of the (bm13 X bm14)F1 hybrid to accept C57BL/6 grafts. Serological studies by direct testing (cytotoxicity and hemagglutination) and by quantitative absorption demonstrated a decrease in the H-2Db private specificity H-2.2 in both bm13 and bm14 when compared to C57BL/6. This was confirmed by SDS-PAGE analysis using antisera detecting the H-2.2 specificity. Attempts to produce antibodies to either the gained or lost specificities of the two mutant strains failed.

Animals↗
PubMed1980

Genetics of histocompatibility in mice. II. Survey for interactions between minor (non-H-2) antigens by skin grafting.

Twenty-five congenic mouse strains differing at distinguishable minor (non-H-2) histocompatibility loci were paired in 71 different combinations. F1 offspring were used as skin-graft donors for more than 4000 recipients to test whether immune responses to parental strain antigens were statistically independent. Thirty-four (48 percent) of the 71 combinations were predicted adequately by an independent response hypothesis. A simple additive model was consistent with 39 (55 percent) of the observed responses, although 18 of these were among those in agreement with the independent hypothesis. A synergistic response faster than that predicted by either the independent or additive response model was seen in 12 (17 percent) of the combinations. The remaining 5 percent were not well described by any of these models. No strain was represented with unusual frequency among those involved in synergistic interactions.

Animals↗
PubMed1980

Interaction of H-2Db with mutant histocompatibility gene H (KH-11) in the mouse.

The detectable presence of H (KH-11)b, a mutant non-H-2 histocompatibility gene, was previously shown to depend upon the simultaneous presence, in the skin-graft donor, of both the mutant gene and the H-2b haplotype. The experiments reported here demonstrate that H-2Db is the essential element of H-2b for this interaction. Of two H-2Db histocompatibility mutations, H-2bm13 can replace H-2Db in this interaction, but H-2bm14 cannot.

Animals↗
PubMed1979

T lymphocyte response to H-2 mutants: cytotoxic effectors are Ly-1+2+.

The lymphocyte differentiation (Ly) antigen phenotype of cytotoxic effector T cells specific for H-2 mutant alloantigens was determined. Cytotoxic effectors generated in primary mixed lymphocyte culture and specific for H-2Kba and H-2Dda alloantigens are sensitive to both anti-Ly-1 and anti-Ly-2 serum plus complement. Reconstitution analysis demonstrated that the mutant-specific T cells were Ly-1+2+. These observations and those previously reported, which indicated that H-2K/D mutant-specific T cells proliferating in mixed lymphocyte culture were Ly-1+2+, demonstrated that Ly-1+2+ T cells are immunocompetent. Furthermore, the nature of the stimulating H-2 complex alloantigen determines the Ly phenotype of responsive T cells.

Animals↗
PubMed1979

An assay for histocompatibility gene mutations in mice.

A method used for detecting histocompatibility gene mutations by tailskin graft tests in mice is described. Advantages and disadvantages are found for this assay system. The results of published work point to some interesting features of the H-gene mutational event, but also leave many questions yet to be answered.

Animals↗
PubMed1978

T-lymphocyte response to H-2 mutants. I. Proliferation is dependent on Ly 1+2+ cells.

We have determined the Ly phenotype of the T lymphocytes which proliferate in response to mutant H-2K and H-2D alloantigens in primary mixed lymphocyte culture. Responder T cells proliferating in reciprocal cultures of H-2d(KdDd) and H-2da(KdDda) lymphocytes were typed Ly 2+ through selective depletion with specific alloantiserum plus complement. Further, B6-Ly 1a lymphocytes proliferating in response to B6-H-2ba and B6-H-2bf stimulators were typed as Ly 1+2+ through similar analysis. These results are discussed with regard to their impact on views of lymphocyte differentiation and factors determining the identity of alloreactive lymphocytes.

Animals↗
PubMed1978

Genetic analyses of differences in incidence of mammary tumors and reticulum cell neoplasms with the use of recombinant inbred lines of mice.

The influence of genes, in addition to genes in the H-2 complex, that effect the genesis of mammary tumors was studied. The recombinant inbred (RI) CXB lines were chosen for this investigation, because they are well suited for the study of the genetics of a trait for which the genotype affects probability of phenotype expression and which therefore is measured as incidence. Females of seven RI lines (CXBD, CXBE, CXBG, CXBH, CXBI, CXBJ, and CXBK) and their progenitor strains C57BL/6By (B6) and BALB/cBy (BALB/c) were given ip injections of MuMTV at 3 months of age and were force bred. They were observed for mammary tumors. The B6 strain was least susceptible, and mammary tumors appeared late in life. The BALB/c strain was most susceptible, and the tumors appeared early in life. The course of tumor development in the RI lines fell between these extremes. The RI strain distribution pattern of mammary tumor incidence indicated that at least one and probably several loci in addition to those at H-2 determined the difference between the BALB/c and B6 strains. Effects of the other gene(s) appeared to be even more important than those of H-2. The locations of those loci were not made clear by this study. The spontaneous incidence of reticulum cell neoplasms was also recorded. The most frequently formed neoplasm of the reticular system was a Hodgkin's-like lesion. The data suggested an influence of the H-2 complex.

Animals↗
PubMed1975

Genetics of susceptibility to plasmacytoma induction. I. BALB/cAnN (C), C57BL/6N (B6), C57BL/Ka (BK), (C times B6)F1, (C times BK)F1, and C times B recombinant-inbred strains.

Plasmacytomas were found in 58% of 373 BALB/cAnN (C) mice given three 0.5-ml doses of mineral oil (Bayol F or light mineral oil) or 2,6,10,14-tetramethylpentadecane (pristane) ip. The incidence of plasmacytomas in C57BL/6N (B6), C57BL/Ka (BK), (C times B6)F1 and (C times BK)F1 was 6.4, 0, 11.5, and 16.5%, respectively. The plasmacytomas occurred in old B6 mice, in contrast to their early appearance in strain C mice. The incidence of plasmacytomas in mineral oil-treated or pristane-treated C times B recombinant-inbred (Rl) strain mice was 28.3% in C times BD, 17.5% IN C times BE, 36.5% IN C times BG, 0% in C times BH, 2.9% in C times Bl, 48% in C times BJ, and 4.3% in C times BK. C times BD, C times BG, and C times BJ strains were considered susceptible to plascytoma induction by mineral oil or pristane; C times BE had a low susceptibility, and C times BH, C times Bl, and C times BK were resistant. The results suggested that there were only a few gene difference between C and B6 or BK that determined susceptibility or resistance to plasmacytoma induction, and that B6 and BK have at least one dominant resistance gene. The distribution pattern of susceptibility and resistance in the C times B Rl strains suggested the presence of a resistance gene on chromosome 9, linkage group II.

Age Factors↗