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  • 17th International Mouse Genome Conference (2003)
    Analysis Nutrition and Metabolic Disease Phenotyping Methods Imaging The Genetics and Genomics of Infectious Disease Verne Chapman Memorial Lecture Table of Contents Sponsor Exhibitor List Awards Photographs POSTER 203 GENETIC MODULATORS OF NATURAL RESISTANCE TO MOUSE CYTOMEGALOVIRUS INFECTION Desrosiers M P University of Ottawa Co Authors Vidal S Institutions University of Ottawa In mice genes of the major histocompatibility complex H2 and the natural killer gene complex NKC determine resistance to cytomegalovirus infection by alternate mechanisms While H2 molecules are thought to act as receptors which modulate infection of individual cells the activating NK cell receptor Ly49H triggers NK cell cytotoxicity against infected cells following engagement of the viral protein m157 We have studied the genetic basis of resistance to infection with CMV in a Mus musculus inbred strain that is highly resistant to MCMV despite the absence of Ly49h We analyzed the inheritance of the resistance phenotype in F2 population Segregation analysis of MCMV resistance follows the bimodal distribution which indicates the presence of several major effector loci in this population Based on sequence analysis a candidate gene for an alternate elicitor of resistance susceptibility to MCMV in this strain has been identified as an activating NK cell receptor

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file251.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Disease Phenotyping Methods Imaging The Genetics and Genomics of Infectious Disease Verne Chapman Memorial Lecture Table of Contents Sponsor Exhibitor List Awards Photographs POSTER 204 HOST DEFENCE AGAINST CYTOMEGALOVIRUS INFECTION IN WILD DERIVED MOUSE STRAINS IS THERE ALLELIC OR GENETIC HETEROGENEITY WITHIN THE Ly49 GENE FAMILY Girard A S University of Ottawa Co Authors 2 Guénet J L 3 Colucci F 4 Vidal S Institutions 2 Pasteur Institute 3 Pasteur Institute 4 University of Ottawa Ly49 genes encode for inhibitory and activating natural killer cell receptors Recently we have shown that Ly49h is the mediator of viral resistance in the C57BL 6 mouse strain All additional inbred strains tested to date lack Ly49h and are susceptible to MCMV Since wild derived strains are separated by many years of evolution from common inbred strains they represent an important source of novel genetic polymorphisms Interestingly clustered in two groups MCMV resistant or MCMV susceptible despite lacking Ly49h As a pre requisite to study the possible role of alternative Ly49 genes in viral resistance in these groups of mice we decided to characterize their Ly49 repertoire We have identified new members of the Ly49 gene family Although the degree of genetic diversity in

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file252.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Biotechnology Co Authors Müller A Lengeling A Chhatwal G S Medina E Institutions GBF German Research Centre for Biotechnology Epidemiological studies revealed that susceptibility to group A streptococcal GAS infection can be influenced by host genetic factors Human major histocompatibility complex MHC genes are genetic determinants of susceptibility to many immunopathological conditions Interestingly mouse strains highly susceptible to GAS infection shared the same H 2 haplotype H 2k while resistant strains display different H 2 haplotypes Based on this observation and the availability of congenic mice from the BALB background carrying the MHC region of susceptible mice BALB k mice we decided to determine the contribution of MHC genes to disease susceptibility to GAS infection For this purpose a comparative study was performed with congenic BALB mice of H 2k BALB k and H 2d BALB c haplotypes which were systemically infected with S pyogenes The more severe outcome of infection in BALB k was associated with high levels of inflammatory cytokines such as IFN γ and IL 12 Since GAS produce several superantigens GAS Sags which seem to be involved in the development of severe infections the potential contribution of GAS SAgs was investigated T cells from BALB k

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file253.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    ANALYSIS OF IMMUNE MECHANISMS IN VDR KO MICE Helming L Research Group Infection Genetics GBF German Research Center for Biotechnology Mascheroder Weg 1 38124 Braunschweig Co Authors 2 Ehrchen J 3 Buer J 3 Probst Kepper M 4 Gunzer M 5 Erben R 6 Balling R 1 Lengeling A Institutions 2 Institute for Experimental Dermatology University of Muenster Roentgenstrasse 21 48149 Muenster 3 Research Group Mucosal Immunity GBF German Research Center for Biotechnology Mascheroder Weg 1 38124 Braunschweig 4 Research Group Immunodynamics GBF German Research Center for Biotechnology Mascheroder Weg 1 38124 Braunschweig 5 Institute of Animal Physiology Ludwig Maximilians University 80539 Munich 6 GBF German Research Center for Biotechnology Mascheroder Weg 1 38124 Braunschweig Host genetic factors have profound influence on infection susceptibility to various pathogens Polymorphisms and mutations in candidate genes have been associated with different outcome of several human infectious diseases One of these candidate genes which is being discussed as a putative infection susceptibility gene is the receptor for Vitamin D3 VDR We used Vdr knockout mice to analyse the role of the Vdr gene in susceptibility to infection The preferred experimental model to study host defense to intracellular bacteria is infection with Listeria monocytogenes We found that Vdr Knockout mice are more susceptible to infection with Listeria This is reflected by decreased survival of Vdr KO mice and a more than ten fold increase of viable Listeria in the livers but not in the spleens of Vdr KO mice as compared to control animals In a second infection model we investigated the resistance of Vdr knockout mice to the intracellular parasite Leishmania major Again we observed reduced resistance of Vdr KO mice against this pathogen as compared to wildtype mice To elucidate the cellular mechanisms behind this impaired host responses we immunized Vdr KO mice

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file254.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    1 Du X 1 Georgel P 2 Janssen E 1 Tabeta K 1 Kim SO 1 Goode J 1 Mann N 1 Mudd S 1 Crozat K 1 Sovath S 1 Han J 1 Beutler B Institutions 1 Scripps Research Institute 2 La Jolla Institute of Allergy and Immunology Using ENU mutagenesis we have examined more than 9 000 mice for defects in responses to Toll like receptor TLR agonists The Lps2 phenotype was identified as a MyD88 independent TLR signaling defect characterized by absence of responses to dsRNA and severe impairment of responses to LPS The existence of Lps2 suggested that TLR3 and TLR4 might share a proximal transducer The mutation was mapped on a total of 1567 meioses and confined to a critical region that encompassed 216 kb of DNA The entire critical region was sequenced by amplifying it in 63 overlapping 4 kb segments The Lps2 mutation was identified as the sole mutational defect within the critical region and was found to be a distal frameshift error in a TIR adapter protein known as TRIF or TICAM 1 Trif Lps2 homozygotes are markedly resistant to the toxic effects of LPS and hypersusceptible to mouse cytomegalovirus failing to

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file255.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Mugambi J 1 Nagda S 1 Gibson J P 2 Wakelin D 1 Baker R L 2 Behnke J Institutions 1 International Livestock Research Institute ILRI P O Box 30709 Nairobi Kenya 2 School of Biological Sciences University of Nottingham Nottingham NG7 2RD U K High resolution mapping of quantitative trait loci QTL to a small genomic interval that allows molecular cloning is not a trivial exercise A number of experimental designs have been proposed to dissect a given QTL including the use of advanced intercross lines AIL which was described by Darvasi and Soller 1995 Recently we have reported the initial mapping of QTL controlling resistance to Heligmosomoides polygyrus in an F 2 crossbred population of resistant SWR and susceptible CBA inbred lines of mice We identified 14 QTL on 12 different chromosomes affecting the parasitological and immunological traits Five of these QTL were associated with two or more traits The QTL were mapped within a relatively large genomic interval of 20 30cM As a step towards fine mapping these QTL we generated 1100 mice which consisted of 500 F6 and 600 F7 SWR x CBA AIL populations and administered the same phenotyping protocol used for the F2 population

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file256.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    1 Vojtíšková J 1 Blažková H 1 Krulová M 1 Pilčík T 1 Krulová M 2 Volf P 3 Demant P Institutions 1 Institute of Molecular Genetics Prague 2 Charles University Prague 3 The Netherlands Cancer Institute Amsterdam Systematic assesment of the role of host genes in clinico pathological and immunological manifestations of Leishmania major induced disease in mice was performed using 20 recombinant congenic RC strains derived from the susceptible and resistant strains BALB c and STS respectively Each RC strain of CcS Dem series carries a different random subsets of 12 5 of genes of the strain STS on the BALB c background This allowed us to study the pathological and immunological characteristics of infected hosts in 20 fixed different random combinations of BALB c and STS genes Disease or healing in different strains occurred in association with different components of immune response with the exception of a frequently occuring correlation between the disease and IgE levels This shows that several patterns of the immune response may be associated with the same clinical outcome depending on the host genotype Linkage analysis of F2 hybrids between the strain BALB c and the RC strains CcS 5 16 and 20

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file257.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    LaCourse R 4 North R J 1 Gros P Institutions 1 Dept of Biochemistry Center for Host Resistance McGill University 2 Biotechnology Research Institute National Research Council 3 Bioinformatics and Statistical Genetics University of Oxford 4 Trudeau institute The mouse DBA 2 strain is very susceptible to infection with virulent Mycobacterium tuberculosis while C57BL 6 is much more resistant This DBA 2 susceptibility includes unrestricted pulmonary microbial replication massive inflammatory response and early death To identify the genes regulating growth of M tuberculosis in the lungs of these two strains 98 informative C57BL 6 X DBA 2 F2 mice were infected by the respiratory route with M tuberculosis H37Rv 200 CFU and the extent of bacterial replication in the lungs at 90 days was used as a quantitative measure of susceptibility in a whole genome scan QTL mapping identified a major locus on chromosome 19 Trl 4 LOD 5 6 which regulated pulmonary replication of M tuberculosis and accounted for 25 of the phenotypic variance An additional effect of a locus Trl 3 previously shown to affect survival to i v infection with M tuberculosis was also noted F2 mice homozygous for C57BL 6 alleles at both Trl 3 and

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file258.shtml (2016-02-17)
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