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W P Lafuse

Publications and source records attributed to W P Lafuse.

At least 37 records · Page 2Linked to original sources
PubMed1993

Stress-associated modulation of proto-oncogene expression in human peripheral blood leukocytes.

Changes in the cellular immune response associated with psychological stress were studied by using an academic stress model with medical students. The authors examined the expression of 2 proto-oncogenes, c-myc and c-myb, in peripheral blood leukocytes (PBLs) obtained from medical students at the time of examinations and at a baseline period approximately 1 month prior to the examinations. The level of messenger ribonucleic acid (mRNA) expression of both protooncogenes was significantly lower in PBLs obtained during examinations than in those from the baseline period. In addition, a significant decrease in the level of mRNA to the glucocorticoid receptor and gamma interferon was also found in the same preparations. The decrease in mRNA content of c-myc, c-myb, the glucocorticoid receptor, and gamma interferon in PBLs obtained from subjects during examinations is consistent with data from previous studies using the same model that have demonstrated a down-regulation of T-lymphocyte activation and proliferation in response to mitogens.

Adult↗
PubMed1992

PFGE mapping and RFLP analysis of the S/D region of the mouse H-2 complex.

We have constructed a long range restriction map of the S/D segment of the mouse H-2 complex by pulsed field gel electrophoresis and hybridization with mouse cDNA probes to Bf and Tnfa genes and human cDNA probes to BAT2, BAT3, BAT4, BAT5, and BAT6 genes which have recently been mapped to the human HLA complex between C2 and HLA-B. The distance between the mouse C2 and Tnfa genes was found to be approximately 350 kilobases. The position of the mouse Bat genes in this map were found to be comparable to the position of the BAT genes in the human HLA complex. A panel of recombinant mouse strains was also examined by restriction fragment analysis with probes detecting the Hsp70, Bat5, and Tnfa genes. The results indicate that recombination in this segment is not random. No recombinants were found with crossovers between the C2 and Hsp70 genes and only one recombinant was found with a crossover between Tnfa and H-2D. In contrast, the crossover sites of 16 recombinants were mapped between the Hsp70 and Tnfa genes. Seven of these recombinants were found to have crossovers between Hsp70 and Bat5 and three recombinants were found to have crossover sites between Bat5 and Tnfa.

Animals↗
PubMed1992

Characterization of ACTH mediated suppression of MHC class II expression by murine peritoneal macrophages.

The effect of ACTH on the expression of major histocompatibility complex (MHC) class II (I-A) glycoprotein by murine peritoneal macrophages was evaluated. ACTH suppressed the expression of I-A by macrophages in a time- and dose-dependent manner. ACTH mediated its effect by decreasing the level of I-A mRNA. ACTH suppressed the expression of I-A by macrophages from mice that are susceptible to the in vivo growth of mycobacteria but did not affect the expression of I-A by macrophages from Mycobacterium bovis strain (BCG)-resistant mice. The concentrations of ACTH required to suppress I-A expression were greater than that required for an effect on adrenal steroid production and may be related to the localized production of ACTH by lymphocytes and macrophages.

Adrenocorticotropic Hormone↗
PubMed1992

Evidence that nucleotide sequence identity is a requirement for meiotic crossing over within the mouse Eb recombinational hot spot.

Meiotic recombination in the mouse is sometimes restricted to specific chromosomal sites. For example, when recombinants within the I region of the mouse major histocompatibility complex (MHC) are examined, the breakpoints between standard alleles can usually be mapped to the Eb gene. DNA sequence analysis of five cases of meiotic crossing over associated with this gene suggests that the recombinational hot spot may be confined to large regions of nucleotide identity located within the second intron of the Eb gene.

Animals↗
PubMed1991

Molecular biology of murine MHC class II genes.

The murine class II genes are contained in the I region of the major histocompatibility complex (MHC). In the mouse, there are seven class II genes: A beta 3, A beta 2, A beta, E beta, E beta 2, A alpha, and E alpha. The A beta and A alpha genes code for the two polypeptide chains that form the I-A immune response molecule. The E beta and E alpha genes code for the two polypeptide chains that form the I-E immune response molecule. This review covers the genetic organization of the I region and the exon-intron structure of the class II genes. This review also discusses site-directed mutagenesis and exon shuffling studies and the effect of these changes on the function of Ia genes. Regulation of the cellular expression of Ia genes is discussed with emphasis on recent studies involving class II transgenic mice. Also, studies mapping recombination hotspots within the E alpha and E beta genes are reviewed.

Animals↗
PubMed1990

Psychological stress-induced modulation of interleukin 2 receptor gene expression and interleukin 2 production in peripheral blood leukocytes.

We explored the expression of the interleukin 2 receptor (IL-2R) and the synthesis of IL-2R messenger RNA by peripheral blood leukocytes obtained from medical students experiencing examination stress in three independent studies. The peripheral blood leukocytes obtained at low-stress baseline periods had significantly higher percentages of IL-2R-positive cells when compared with cells obtained from the same individuals during examinations. In addition, IL2-R messenger RNA in peripheral blood leukocytes decreased significantly during examination periods in a subset of 13 subjects. In one study, we found an increase in the accumulation of interleukin 2 in cultures of cells showing down regulation of IL-2R expression and IL-2R messenger RNA levels. While there are ample data demonstrating stress-associated decrements in the immune response in humans and animals, these data provide the first evidence that this interaction may be observed at the level of gene expression. The data suggest one mechanism whereby the central nervous system modulates the immune response during psychological stress.

Adult↗
PubMed1990

Molecular analysis of two recombinant mouse strains with crossovers in the E alpha recombination hot spot.

Recombination in the E alpha gene of the mouse major histocompatibility complex has been found to occur only in mice derived from crosses between strains with the k and p haplotypes. In the present paper the crossover sites of six additional strains were examined by RFLP analysis. These recombinant strains were derived from crosses between strains (B10.RPD1, B10.RPD2) with crossovers in the E alpha gene and B10.M (H-2f). Four have crossover sites between the E alpha gene and the S region. One recombinant (B10.RFD7) also crossed over within the E alpha gene and a second (B10.RPF1) crossed over within a segment located to the left of the E alpha gene. This study suggests that the DNA sequence responsible for recombination in the E alpha gene is also present in the B10.RPD1 and B10.RPD2 recombinant strains.

Animals↗
PubMed1987

Identification of I-E alpha genes in H-2 recombinant mouse strains by F1 complementation.

Nine recombinant H-2 mouse strains with crossovers in the I region between I-E-negative haplotypes f,q and I-E-positive haplotypes p,k were examined for I-E expression by microcytotoxicity dye exclusion assay. These recombinants were found to be negative for I-E expression. There are two possible genotypes in these recombinant mouse strains that could result in lack of I-E expression. Recombinants with crossovers between the E alpha gene and the S region would have both nonexpressed I-E alpha and beta genes (E beta fE alpha f, E beta qE alpha q) and recombinants with crossovers between the E beta and E alpha genes would have a nonexpressed E beta gene (E beta f or E alpha q) and a functional E alpha gene (E alpha k or E alpha p). To distinguish between these possible genotypes these recombinants were crossed to B10.A(4R), which carries a functional E alpha k gene but is I-E-negative due to a nonexpressed E alpha b gene. F1 mice were examined for transcomplementing I-E molecules by immunoprecipitation of 3H-leucine-radiolabeled detergent lysates of spleen cells with a monoclonal I-E antibody (14-4-4). Detection of a transcomplementing I-E molecule was confirmed by immunoprecipitation with a monoclonal antibody (H9-14.8) specific for the I-Ek beta polypeptide chain derived from B10.A(4R) and by tryptic peptide map comparisons. Five recombinant mouse strains were able to complement with B10.A(4R) in F1 mice to generate a transcomplementing I-E molecule, and thus have an expressed I-E alpha gene (E alpha k or E alpha p). Four recombinants did not complement with B10.A(4R) in the F1 expression of I-E molecules, and thus have nonexpressed I-E alpha genes (E alpha f or E alpha q).

Animals↗
PubMed1986

Mapping of a second recombination hot spot within the I-E region of the mouse H-2 gene complex.

The crossover points of nine intra-I region recombinant mouse strains were determined by restriction fragment analysis. The recombinants were examined for the presence of k and p haplotype specific DNA restriction endonuclease sites. These restriction sites were a Sac I site between the E beta and E beta 2 genes, a Hpa I site within the E beta 2 gene, and a Rsa I site approximately 1 kb to the right of the E alpha gene. Seven of the recombinants were found to have crossovers between the Hpa I and the Rsa I site. This analysis suggests that a recombination hot spot exists within this segment. This segment is approximately 12-14 kb, and contains the E alpha gene and the intervening sequence between the E beta 2 and E alpha genes.

Animals↗
PubMed1986

Recombination hot spots within the I region of the mouse H-2 complex map to the E beta and E alpha genes.

Recombinant mouse strains with crossovers in the I region of the H-2 major histocompatibility complex were examined by restriction fragment analysis for the presence of polymorphic restriction sites within the E beta and E alpha genes. Nine recombinant mouse strains were shown to have crossed over within a 5 kb DNA segment that contains the large intron between the second and third exons of the E beta gene. These results are in accord with previous studies mapping a recombination hot spot within this gene. Seven recombinant mouse strains between the p and k haplotypes were shown to have crossed over in a 6 kb segment within the E alpha gene. These results show the existence of a recombination hot spot within the E alpha gene. Comparison of the H-2 haplotypes involved in these two recombination hot spots suggests that a specific DNA sequence in b, s, f, and q haplotypes may act to promote recombination in the E beta gene and a specific DNA sequence in the p haplotype may act to promote recombination in the E alpha gene.

Animals↗
PubMed1986

Serological confirmation in Ia mutant B6.C-H-2bm12 of gene conversion.

Recently it has been suggested that a short segment of the DNA sequence of the Ia beta gene in the mutant B6.C-H-2bm12 (bm12) is derived from the Eb beta gene by a gene-conversion-like mechanism, and that the same segment is also seen in the Ek beta gene. To obtain serological evidence for this idea, we produced an antibody against the "new" determinant on the I-Abm12 molecule by immunizing A.BY mice with bm12 cells. After absorption with B6 lymphocytes to remove antibodies against background antigens, the antisera lysed bm12 cells. Typical Ia peaks were obtained by immunoprecipitation. The absorbed antiserum reacted with B10.A (Ek beta), B10.A(5R) (Eb beta) and B10.S(9R) (Es beta), but not B10. The unabsorbed antiserum is specific for Ia when tested on A background mice. The antiserum lysed spleen cells of Ik strains (A/Sn, A.AL, A.TBR1, and A.TFR1) but not Ak strain, A.TBR13 (KsAkEbSbDb), confirming the presence of antibodies against the I-Ek molecule. This anti-serum also lysed the cells from (A.BY X A.TFR5)F1, which expresses the transcomplementing Eb beta Ek alpha molecule and from the (A.SW X A.TFR5)F1 which expresses the transcomplementing Es beta Ek alpha molecule. These data are consistent with DNA sequence analyses, and show the existence of a determinant (Ia.51) generated in the bm12 mutant by a gene-conversion-like event that is also present in the I-Ek, I-Eb, and I-Es beta polypeptide chains.

Animals↗
PubMed1986

Partial suppression of Theiler's virus-induced demyelination in vivo by administration of monoclonal antibodies to immune-response gene products (Ia antigens).

In vivo administration of monoclonal antibody reactive with major histocompatibility complex-encoded Ia molecules (I-As) partially suppressed inflammation and demyelination in the spinal cord of SJL/J (H-2s) mice persistently infected with Theiler's murine encephalomyelitis virus. Demyelination was decreased if antibody was given at the time of virus inoculation or after inflammation had been established in the spinal cord. The decrease in demyelination was independent of isolation of infectious virus from the CNS or of serum titers of immunoglobulin to purified viral antigen. Thus, Theiler's virus-induced demyelination is mediated, in part, by immune cells that carry Ia class II molecules.

Agglutination Tests↗
PubMed1986

Molecular heterogeneity of I-Ab molecules: analysis of I-Ab subsets with monoclonal antibodies.

In the mouse there are two Ia molecules, A and E, which are encoded by two alpha genes and two beta genes. However, previous studies from this laboratory suggested the existence of multiple forms of Ia molecules. In this report, we have investigated the molecular heterogeneity of Ab molecules by isolating and analyzing subpopulations of Ia molecules. By using monoclonal antibody affinity columns, we have isolated four distinct subpopulations of Ab molecules. These subpopulations representing a significant fraction of the total A molecules were negative for determinants recognized by one or more anti-Ab monoclonal antibodies. Possible mechanisms of the origin of these molecules are discussed.

Animals↗