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Biomedical subjects

C M Warner

Publications and source records attributed to C M Warner.

At least 91 records · Page 5Linked to original sources
PubMed1983

Genetic variability at the pig SLA complex in U.S. breeds of pigs.

Lymphocytes from 90 mature pigs and 548 growing pigs from 65 litters were screened with cytotoxic antibodies against swine lymphocyte antigens. Pigs included in the survey were from the Chester White, Duroc, Hampshire, Landrace and Yorkshire breeds. Significant differences between breeds were found in the frequency of the three haplotypes tested. Such differences may provide the genetic variability needed to determine associations between disease susceptibility and the pig's major histocompatibility gene complex.

Animals↗
PubMed1983

Genetic control of the immune response to human adult haemoglobin (HbA1) and sickle cell haemoglobin (HbS).

The humoral response of twelve strains of mice to immunization with either normal adult human haemoglobin (HbA1) or sickle-cell haemoglobin (HbS) was studied using a quantitative enzyme-linked immunosorbant assay (ELISA). Results indicate the presence of at least two genes that control the magnitude of this response, one of which is located at the 'D-end' of the H-2 complex. H-2 haplotypes s, q and k are associated with a low response, haplotypes d and a with a high response, and the b haplotype with an intermediate response. No difference in the pattern or magnitude of the response was observed when HbS was used as the immunogen in place of HbA1. The N-terminal octapeptides of the beta chains of HbA1 and HbS were synthesized and the presence of antibodies specific for the N-terminal octapeptides was tested. The magnitude of the anti-N-terminal response correlated with that to the intact molecules with one exception. A much lower response to the beta s-peptide was found in the C57BL/10Sn mice. Monoclonal antibodies were prepared to HbA1 and HbS. Three clones were studied for their reaction with HbA1, HbS, and the beta A1 and beta S peptides. One clone was found which binds both the beta A1 and beta S peptides. This indicates that the N-terminal portion of the beta chain of human haemoglobin is antigenic in mice.

Amino Acid Sequence↗
PubMed1982

Detection of H-2 antigens on 8-cell mouse embryos.

H-2 antigens were detected on 80-cell mouse embryos of the b, k, and d haplotypes, but not on 8-cell embryos of the a haplotype. The technique used for detection of H-2 antigens on the embryos was a highly sensitive, automated, complement-dependent cytotoxicity assay, based on the principle that live embryos will incorporate 3H-thymidine into DNA, but embryos killed with antiserum and complement will not. The amount of H-2 present on 8-cell embryos is apparently less than that present on blastocysts. A possible function of H-2 antigens in development is proposed.

Animals↗
PubMed1982

Role of the H-2 complex in preimplantation mouse embryo development.

The H-2 complex was found to influence early mouse embryo development. Slow development was shown to be associated with the H-2k haplotype. By the use of congenic strains, it was clearly demonstrated that gene(s) in the H-2 complex affect the time of the first cleavage division and the rate of subsequent preimplantation development

Animals↗
PubMed1982

Genes affect the timing of early mouse embryo development.

The rate of preimplantation mouse embryo development was found to be influenced by genes both within and outside the H-2 complex. An H-2 associated gene, called Ped, was shown to govern either fast or slow development. Analysis of congenic strains on a C57BL/10Sn background showed that fast development is associated with the b, d, q, s, and u haplotypes, whereas slow development is associated with the k and r haplotypes. Analysis of the recombinant haplotype, a suggested that the fast Ped gene maps to the D end of the H-2 complex. The study of congenic strains on a BALB/c background has shown that background genes, as well as the H-2 associated Ped gene, play a role in the control of the rate of early embryonic cleavage.

Animals↗
PubMed1982

Genetic analysis of H-2 linked gene(s) affecting early mouse embryo development.

The number of cells in preimplantation mouse embryos of different H-2 haplotypes was analysed. It was found that embryos of the H-2k haplotype have fewer cells per embryo than those of the H-2b haplotype. By analysing reciprocal congenic pairs of mice it was demonstrated unequivocally that slow development is linked to the H-2k haplotype and fast development to the H-2b haplotype. The gene (s) in the H-2 complex which influence early mouse embryo development have been named Ped: preimplantation embryo development. Analysis of F1 hybrid embryos showed that fast development is dominant. Reciprocal F1 crosses yielded identical results, which indicated there was no apparent effect of the maternal egg cytoplasm on Ped gene expression. Analysis of F2, and back-cross embryos was consistent with the interpretation that there is a major gene located in the H-2 complex (Ped), which is modified by environment and genetic background, that influences early mouse embryo development.

Animals↗
PubMed1982

The immune response of allophenic mice to the synthetic polymer GL phi. III. Allotype analysis of anti-GL phi antibody.

Allophenic mice produced by aggregating 8-cell embryos from a low responder (CBA) and a high responder (DBA/1) strain to the synthetic amino acid polymer GL phi.. In some strains of mice the immune response to this polymer is controlled by two genes, alpha and beta, which map to the IE/C and IA subregions of the H-2 complex, respectively. The CBA strain is alpha+beta--whereas the DBA/1 strain can be considered to be alpha+beta+. These two strains also differ in immunoglobulin allotype: CBA is allotype alpha and DBA/1 is allotype c. Eight CBA--DBA/1 allophenic mice were immunized with GL phi.. Four of the mice gave a high secondary response to the polymer. The allotype of the antibody from these mice was determined by affinity chromatography, and it was found that only allotype c was present. This means that all of the antibody was produced by high responder DBA/1 cells. Thus, there is no evidence for the cooperation of histoincompatible cells in the mounting of an immune response by allophenic mice.

Animals↗
PubMed1981

Specificity of H-2 antigens expressed on mouse blastocysts.

A highly sensitive cytotoxicity assay was used to detect H-2 antigens on mouse blastocyst stage embryos of the b, a, k, and d haplotypes. The assay was based on the principle that live embryos incorporate 3H-thymidine into DNA whereas embryos killed with antiserum and complement do not. The use of specific alloantisera showed that blastocysts of different haplotypes express different H-2 antigens. Thus, positive evidence was obtained for the expression of Kd and Dk molecules and negative evidence for the expression of Db, Kk, and Dd molecules. Evidence was also obtained that blastocysts express different H-2 antigens than those found on adult lymphocytes. Unexpected cross-reactions were found when some of the alloantisera were tested on blastocysts of different haplotypes. It is proposed that the aberrant expression of H-2 antigens on embryos might facilitate their escape from surveillance by the maternal immune system.

Animals↗
PubMed1980

Genetic control of the immune response of mice to highly dinitrophenylated human gamma-globulin (DNP56HGG).

The immune response to highly dinitrophenylated human gamma-globulin (DNP56HGG) was tested in inbred strains of mice. Significant differences in the anti-DNP response among inbred strains were found, including the magnitude of serum antibody and the location of plaque-forming cells (spleen or lymph nodes). The strain differences persisted when the dose and adjuvant were changed. The genetic control of the anti-DNP response to DNP56HGG was investigated. The analysis of the response of congenic and F1 hybrid mice to DNP56HGG suggests that at least two genes are involved in the control of the anti-DNP response. The two genes are demonstrated by complementation in the F1 generation, and show no correlation with H-2 haplotype or IgG2a allotype. A third gene may be implicated by differences in response observed between male and female mice.

Adjuvants, Immunologic↗
PubMed1978

The immune response of allophenic mice to 2,4-dinitrophenyl (DNP)-bovine gamma globulin. I. Allotype analysis of anti-DNP antibody.

The question of whether or not lymphoid cells can cooperate across a histocompatibility difference barrier has been studied in several laboratories. Using an adoptive transfer system, Katz et al. (1) first showed that T cells from (low responder x high responder) F(1) mice, primed to the terpolymer L-glutamic acid, L-lysine, L-tyrosine (GLT), could collaborate with 2,4-dinitrophenyl (DNP)-primed B cells from a high responder, but not a low responder strain, in response to DNP-GLT. The response to GLT is under H- 2-1inked Ir gene control. In contrast, studies with mouse bone marrow chimeras have shown that T cells can interact with H-2-histoincompatible B cells in response to antigens not under Ir gene control (2-4). Another type of chimera, the allophenic mouse, has been used to study possible histoincompatible cell interactions to a number of antigens, including DNP-L- glutamic acid, L-lysine, L-alanine; L-glutamic acid, L-alanine, L-tyrosine; L-glutamic acid, L-lysine, L-phenylalanine; and poly-L (Tyr, Glu)-poly D,L- Ala-poly-L-Lys[T,G)-A-L] (5-9). The response to each of these antigens is under H-2-1inked Ir gene control. It was initially reported (8, 9) that in allophenic mice containing both high and low responder cells, the antibody to (T,G)-A-L was of both the high and low responder allotype. This was interpreted to mean that high responder T cells had cooperated with low responder B cells across a histocompatibility difference barrier in the environment of the allophenic mice. However, Press and McDevitt (10) have recently reported that additional and more accurate analyses of these allophenic mouse sera failed to detect any anti-(T,G)-A-L antibody of the low responder allotype. Moreover, in an experiment using bone marrow chimeras, there was no low responder allotype antibody produced in response to (T,G)-A- L(10). The present study was undertaken to test the immune response of allophonic mice to an antigen, DNP-bovine gamma globulin (DNP(56)BGG), known to be controlled by genes both inside and outside the H-2 complex (11, 12).(1) When high and low responder cells to DNP(56)BGG are present in allophenic mice, only antibody of the high responder allotype is produced. The results suggest that cell cooperation in allophenic mice cannot occur across a histocompatibility difference barrier in response to an antigen whose genetic control is at least partially within the H-2 complex.

Animals↗
PubMed1978

Quantitative analysis of spleen cell and immunoglobulin allotype composition of (CBAxCBA/H-T6) in equilibrium C57BL/6 allophenic mice.

Fifteen (CBAxCBA/H-T6) in equilibrium C57BL/6 allophenic mice were analyzed for the parental composition of their spleen white blood cells and serum immunoglobulin allotypes. The spleen compositions, assessed by a microcytotoxicity test, showed that the animals covered a range of parental cell mixtures. The allotype compositions of the IgG2a and IgG2b subclasses were determined by a solid phase radioimmunoassay. Although the absolute amount of IgG2a and IgG2b varied markedly from animal to animal, the percentage of the two allotypes in each subclass was remarkably constant. This suggests that the synthesis of IgG2a and IgG2b may be under a coordinate control system. Also, the spleen cell compositons were in excellent agreement with both the IgG2a and IgG2b subclass compositions. The quantitative analysis of the immune systems of allophenic mice may be first step toward the understanding of the mechanisms of tolerance of histoincompatible cells in allophenic mice.

Animals↗
PubMed1977

Chimeric drift in allophenic mice.

The composition of the immune system of 33 allophenic mice of four different types [C57BL/6 in equilibrium DBA/1, C57BL/6 in equilibrium (CBA X CBA/H-T6), C57BL/6 in equilibrium (A X SJL), DBA/1 in equilibrium (CBA X CBA/H-T6)] was studied. It was found that the parental composition of the peripheral white blood cells changed significantly during a two-month interval in 11/33 or 33% of the mice studied. This phenomenon has been termed chimeric drift. The animals were sacrificed between 9 and 16 months of age, and the parental composition of the peripheral white blood cells, spleen white blood cells, and thymocytes was determined on the day of sacrifice. It was foound that the peripheral white blood cell and spleen white blood cell compositions showed a high degree of correlation. However 8/33 or 24% of the mice studied showed discordance of the spleen and thymocyte cell populations. Seven of the 8 mice which showed spleen-thymocyte discordance, had also shown evidence of chimeric drift earlier in their lives. We suggest that this is evidence that chimeric drift may have an immunological basis.

Animals↗
PubMed1977

The immune response of allophenic mice to the synthetic polymer L-glutamic acid, L-lysine, L-phenylalanine. II. Lack of gene complementation in two nonresponder strains.

The genetic control of the immune response of inbred strains of mice to certain antigens has been demonstrated to be governed by a set of Ir genes linked to the major histocompatibility complex (H-2) of mice (1,2). Until recently, the control was thought to be governed by single, dominant genes, located within the I region of the H-2 complex. Merryman et al. (3) originally demonstrated that the immune response to the synthetic terpolymer L-glutamic acid, L-lysine, L-phenylaline (GLphi) is under dominant, H-2-linked Ir gene control (4-7). This was shown both by crossing two nonresponder parental strains to produce responder offspring in the F(1) generation, and by the analysis of appropriate recombinant stains of mice. The two complementing genes have been mapped in the IA and IC regions of the H-2 complex, and have been termed beta and alpha, respectively (5,6). Thus, any strain of mouse may contain neither, one, or both genes. Only mice containing both genes are capable of responding to GLphi. It has been shown using F(1) hybrid and recombinant strains of mice, that the alpha- and beta-genes can complement each other in either the cis (on the same chromosome) or in the trans (on different chromosomes) position (8). In this paper we report the results of studies aimed at answering the question of whether or not the alpha- and beta- genes can complement each other when they are present in different lymphoid cells. To this end we have constructed allophenic mice composed of two nonresponder strains (A and C57BL/6), which show gene complementation in the F(1) generation. Allophenic mice are chimeras containing two cell types coexisting in a "normal" environment. The mice were tested for the specific cellular composition of the two parental cell types and were found to possess a complete range in the relative proportion of the two cell types. This report demonstrates that regardless of the mixture of cell types present in the allophenic mice, none of them were responders to GLphi. Thus no complementation of the alpha- and beta-genes is seen when the two genes are present in different cells.

Animals↗