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Judith A Whittumhudson - One of the best experts on this subject based on the ideXlab platform.

  • pathoGenesis of autoimmune lacrimal gland disease in mrl mpj mice
    Advances in Experimental Medicine and Biology, 2002
    Co-Authors: Douglas A. Jabs, R A Prendergast, Judith A Whittumhudson
    Abstract:

    MRL/MpJ mice spontaneously develop lacrimal and salivary gland inflammation and are a model for the human disorder Sjogren’s syndrome. 1-3 Two congenic substrains of MRL/MpJ mice exist, MRL/MpJ-+/+ (MRL/+) andMRL/MpJ-lpr/lpr(MRL/lpr). These substrains differ only at a single Autosomal Recessive Gene locus, the1prmutation. This mutation results in altered Fas protein, defective lymphocyte apoptosis, defective clonal deletion of autoreactive T-cells in peripheral lymphoid organs and accelerated autoimmune disease in MRL/lpr mice when compared to MRL/+ mice. 4.5 MRL/lpr mice typically die at 6 months of age, whereas MRL/+ mice often live to 2 years. Both substrains develop lacrimal gland inflammation, although the lacrimal gland disease develops earlier in MRL/lpr than MRL/+ mice, and at comparable ages, MRL/lpr mice have more severe and extensive disease.3 ; The lacrimal gland lesions in both substrains are composed largely of T-cells (approximately 80%), the majority of which are CD4+ T-cells. Lesser numbers of CD8+ T-cells, B-cells and macrophages are present. In aged (18-month) MRL/+, mice B-cells accumulate in the lacrimal gland lesions.2.3.6

  • the role of fas fas ligand mediated apoptosis in autoimmune lacrimal gland disease in mrl mpj mice
    Investigative Ophthalmology & Visual Science, 2001
    Co-Authors: Douglas A. Jabs, Judith A Whittumhudson, Bella Lee, R A Prendergast
    Abstract:

    PURPOSE. MRL/MpJ mice spontaneously develop lacrimal gland inflammation and are a model for the human disorder Sjogren's syndrome. MRL/MpJ-lpr/lpr (MRL/lpr) and MRL/Mp-1/1 (MRL/1) mice are congenic substrains, which differ only by a single Autosomal Recessive Gene, the lpr mutation. This muta- tion results in defective Fas protein, defective lymphocytic apoptosis, and accelerated autoimmune lacrimal gland disease in MRL/lpr mice. We evaluated apoptosis in the lacrimal glands of MRL/lpr and MRL/1 mice. METHODS. Inflammatory cells in the lacrimal glands of MRL/lpr and MRL/1 mice were evaluated for apoptosis with TUNEL staining and Fas and Fas ligand expression with immunohisto- chemistry. RESULTS. MRL/lpr mice had a greater percentage of the lacrimal gland replaced by inflammatory infiltrate (30.3% 6 7.0%) than did MRL/1 mice (13.0% 6 3.0%, P 5 0.02). However, similar amounts of lymphocytic apoptosis were present in the lacrimal glands of MRL/lpr and MRL/1 mice. The mean number of apoptotic cells per unit area of inflammation was 23.8 6 2.4 in MRL/lpr mice and 24.6 6 6.0 in MRL/1 mice (P 5 0.91). Fas expression was absent on lymphocytes in MRL/lpr mice but was present on lymphocytes in MRL/1 mice. Fas ligand ex- pression was present on epithelial structures in both sub- strains. CONCLUSIONS. The accelerated lacrimal gland disease inflamma- tion in MRL/lpr mice does not appear to be due to decreased apoptosis in the microenvironment of the lacrimal gland of MRL/lpr mice. It appears that in MRL/lpr mice there is defec- tive extrathymic lymphoid apoptosis, permitting a relatively greater expansion of autoreactive T cells, which subsequently invade the lacrimal gland. (Invest Ophthalmol Vis Sci. 2001;42: 399 - 401)

R A Prendergast - One of the best experts on this subject based on the ideXlab platform.

  • pathoGenesis of autoimmune lacrimal gland disease in mrl mpj mice
    Advances in Experimental Medicine and Biology, 2002
    Co-Authors: Douglas A. Jabs, R A Prendergast, Judith A Whittumhudson
    Abstract:

    MRL/MpJ mice spontaneously develop lacrimal and salivary gland inflammation and are a model for the human disorder Sjogren’s syndrome. 1-3 Two congenic substrains of MRL/MpJ mice exist, MRL/MpJ-+/+ (MRL/+) andMRL/MpJ-lpr/lpr(MRL/lpr). These substrains differ only at a single Autosomal Recessive Gene locus, the1prmutation. This mutation results in altered Fas protein, defective lymphocyte apoptosis, defective clonal deletion of autoreactive T-cells in peripheral lymphoid organs and accelerated autoimmune disease in MRL/lpr mice when compared to MRL/+ mice. 4.5 MRL/lpr mice typically die at 6 months of age, whereas MRL/+ mice often live to 2 years. Both substrains develop lacrimal gland inflammation, although the lacrimal gland disease develops earlier in MRL/lpr than MRL/+ mice, and at comparable ages, MRL/lpr mice have more severe and extensive disease.3 ; The lacrimal gland lesions in both substrains are composed largely of T-cells (approximately 80%), the majority of which are CD4+ T-cells. Lesser numbers of CD8+ T-cells, B-cells and macrophages are present. In aged (18-month) MRL/+, mice B-cells accumulate in the lacrimal gland lesions.2.3.6

  • the role of fas fas ligand mediated apoptosis in autoimmune lacrimal gland disease in mrl mpj mice
    Investigative Ophthalmology & Visual Science, 2001
    Co-Authors: Douglas A. Jabs, Judith A Whittumhudson, Bella Lee, R A Prendergast
    Abstract:

    PURPOSE. MRL/MpJ mice spontaneously develop lacrimal gland inflammation and are a model for the human disorder Sjogren's syndrome. MRL/MpJ-lpr/lpr (MRL/lpr) and MRL/Mp-1/1 (MRL/1) mice are congenic substrains, which differ only by a single Autosomal Recessive Gene, the lpr mutation. This muta- tion results in defective Fas protein, defective lymphocytic apoptosis, and accelerated autoimmune lacrimal gland disease in MRL/lpr mice. We evaluated apoptosis in the lacrimal glands of MRL/lpr and MRL/1 mice. METHODS. Inflammatory cells in the lacrimal glands of MRL/lpr and MRL/1 mice were evaluated for apoptosis with TUNEL staining and Fas and Fas ligand expression with immunohisto- chemistry. RESULTS. MRL/lpr mice had a greater percentage of the lacrimal gland replaced by inflammatory infiltrate (30.3% 6 7.0%) than did MRL/1 mice (13.0% 6 3.0%, P 5 0.02). However, similar amounts of lymphocytic apoptosis were present in the lacrimal glands of MRL/lpr and MRL/1 mice. The mean number of apoptotic cells per unit area of inflammation was 23.8 6 2.4 in MRL/lpr mice and 24.6 6 6.0 in MRL/1 mice (P 5 0.91). Fas expression was absent on lymphocytes in MRL/lpr mice but was present on lymphocytes in MRL/1 mice. Fas ligand ex- pression was present on epithelial structures in both sub- strains. CONCLUSIONS. The accelerated lacrimal gland disease inflamma- tion in MRL/lpr mice does not appear to be due to decreased apoptosis in the microenvironment of the lacrimal gland of MRL/lpr mice. It appears that in MRL/lpr mice there is defec- tive extrathymic lymphoid apoptosis, permitting a relatively greater expansion of autoreactive T cells, which subsequently invade the lacrimal gland. (Invest Ophthalmol Vis Sci. 2001;42: 399 - 401)

Douglas A. Jabs - One of the best experts on this subject based on the ideXlab platform.

  • pathoGenesis of autoimmune lacrimal gland disease in mrl mpj mice
    Advances in Experimental Medicine and Biology, 2002
    Co-Authors: Douglas A. Jabs, R A Prendergast, Judith A Whittumhudson
    Abstract:

    MRL/MpJ mice spontaneously develop lacrimal and salivary gland inflammation and are a model for the human disorder Sjogren’s syndrome. 1-3 Two congenic substrains of MRL/MpJ mice exist, MRL/MpJ-+/+ (MRL/+) andMRL/MpJ-lpr/lpr(MRL/lpr). These substrains differ only at a single Autosomal Recessive Gene locus, the1prmutation. This mutation results in altered Fas protein, defective lymphocyte apoptosis, defective clonal deletion of autoreactive T-cells in peripheral lymphoid organs and accelerated autoimmune disease in MRL/lpr mice when compared to MRL/+ mice. 4.5 MRL/lpr mice typically die at 6 months of age, whereas MRL/+ mice often live to 2 years. Both substrains develop lacrimal gland inflammation, although the lacrimal gland disease develops earlier in MRL/lpr than MRL/+ mice, and at comparable ages, MRL/lpr mice have more severe and extensive disease.3 ; The lacrimal gland lesions in both substrains are composed largely of T-cells (approximately 80%), the majority of which are CD4+ T-cells. Lesser numbers of CD8+ T-cells, B-cells and macrophages are present. In aged (18-month) MRL/+, mice B-cells accumulate in the lacrimal gland lesions.2.3.6

  • the role of fas fas ligand mediated apoptosis in autoimmune lacrimal gland disease in mrl mpj mice
    Investigative Ophthalmology & Visual Science, 2001
    Co-Authors: Douglas A. Jabs, Judith A Whittumhudson, Bella Lee, R A Prendergast
    Abstract:

    PURPOSE. MRL/MpJ mice spontaneously develop lacrimal gland inflammation and are a model for the human disorder Sjogren's syndrome. MRL/MpJ-lpr/lpr (MRL/lpr) and MRL/Mp-1/1 (MRL/1) mice are congenic substrains, which differ only by a single Autosomal Recessive Gene, the lpr mutation. This muta- tion results in defective Fas protein, defective lymphocytic apoptosis, and accelerated autoimmune lacrimal gland disease in MRL/lpr mice. We evaluated apoptosis in the lacrimal glands of MRL/lpr and MRL/1 mice. METHODS. Inflammatory cells in the lacrimal glands of MRL/lpr and MRL/1 mice were evaluated for apoptosis with TUNEL staining and Fas and Fas ligand expression with immunohisto- chemistry. RESULTS. MRL/lpr mice had a greater percentage of the lacrimal gland replaced by inflammatory infiltrate (30.3% 6 7.0%) than did MRL/1 mice (13.0% 6 3.0%, P 5 0.02). However, similar amounts of lymphocytic apoptosis were present in the lacrimal glands of MRL/lpr and MRL/1 mice. The mean number of apoptotic cells per unit area of inflammation was 23.8 6 2.4 in MRL/lpr mice and 24.6 6 6.0 in MRL/1 mice (P 5 0.91). Fas expression was absent on lymphocytes in MRL/lpr mice but was present on lymphocytes in MRL/1 mice. Fas ligand ex- pression was present on epithelial structures in both sub- strains. CONCLUSIONS. The accelerated lacrimal gland disease inflamma- tion in MRL/lpr mice does not appear to be due to decreased apoptosis in the microenvironment of the lacrimal gland of MRL/lpr mice. It appears that in MRL/lpr mice there is defec- tive extrathymic lymphoid apoptosis, permitting a relatively greater expansion of autoreactive T cells, which subsequently invade the lacrimal gland. (Invest Ophthalmol Vis Sci. 2001;42: 399 - 401)

D O F Skibinski - One of the best experts on this subject based on the ideXlab platform.

  • sex determination in the genus oreochromis 1 sex reversal gynoGenesis and triploidy in o niloticus l
    Theoretical and Applied Genetics, 1991
    Co-Authors: G C Mair, A G Scott, D J Penman, J A Beardmore, D O F Skibinski
    Abstract:

    Sex ratios from 62 single-pair matings of normal broodstock O. aureus were highly heteroGeneous with an overall deficit of males (41.4%). Peaks in the sex ratio frequency distribution occurred at 1∶1, 3∶5 and 1∶3 (male∶female). Hybridisation of O. aureus with O. mossambicus, O. spilums and O. niloticus produced highly variable sex ratios, suggesting a complexity of hybrid sex determination. Few valid inferences could be made regarding intraspecific sex determination from these hybrid data. Sex ratios from progeny testing of sex-reversed males (1∶3) and most sex-reversed females (1∶0) provide evidence for female heterogamety in O. aureus. Several aberrant ratios observed suggest Mendelian inheritance of an Autosomal Recessive Gene (F,f), epistatic to the major sex-determining Gene (W,Z). Sex ratios of triploids and gynogens support the hypothesis of recombination between the centromere and the major sex-determining locus. Progeny testing of a female mitogyne demonstrated the viability of a novel WW “superfemale”, which gave only female offspring. Not all data could be explained by a two-factor model of sex determination. Further exceptional sex ratios may be accounted for by rare Autosomal or environmental sex-modifying factors. It is concluded that O. aureus has a multifactorial mechanism of sex determination with the underlying primary mechanism of female heterogamety.

  • sex determination in the genus oreochromis 2 sex reversal hybridisation gynoGenesis and triploidy in o aureus steindachner
    Theoretical and Applied Genetics, 1991
    Co-Authors: G C Mair, A G Scott, D J Penman, D O F Skibinski, J A Beardmore
    Abstract:

    Sex ratios from 62 single-pair matings of normal broodstock O. aureus were highly heteroGeneous with an overall deficit of males (41.4%). Peaks in the sex ratio frequency distribution occurred at 1∶1, 3∶5 and 1∶3 (male∶female). Hybridisation of O. aureus with O. mossambicus, O. spilums and O. niloticus produced highly variable sex ratios, suggesting a complexity of hybrid sex determination. Few valid inferences could be made regarding intraspecific sex determination from these hybrid data. Sex ratios from progeny testing of sex-reversed males (1∶3) and most sex-reversed females (1∶0) provide evidence for female heterogamety in O. aureus. Several aberrant ratios observed suggest Mendelian inheritance of an Autosomal Recessive Gene (F,f), epistatic to the major sex-determining Gene (W,Z). Sex ratios of triploids and gynogens support the hypothesis of recombination between the centromere and the major sex-determining locus. Progeny testing of a female mitogyne demonstrated the viability of a novel WW "superfemale", which gave only female offspring. Not all data could be explained by a two-factor model of sex determination. Further exceptional sex ratios may be accounted for by rare Autosomal or environmental sex-modifying factors. It is concluded that O. aureus has a multifactorial mechanism of sex determination with the underlying primary mechanism of female heterogamety.

J A Beardmore - One of the best experts on this subject based on the ideXlab platform.

  • sex determination in the genus oreochromis 1 sex reversal gynoGenesis and triploidy in o niloticus l
    Theoretical and Applied Genetics, 1991
    Co-Authors: G C Mair, A G Scott, D J Penman, J A Beardmore, D O F Skibinski
    Abstract:

    Sex ratios from 62 single-pair matings of normal broodstock O. aureus were highly heteroGeneous with an overall deficit of males (41.4%). Peaks in the sex ratio frequency distribution occurred at 1∶1, 3∶5 and 1∶3 (male∶female). Hybridisation of O. aureus with O. mossambicus, O. spilums and O. niloticus produced highly variable sex ratios, suggesting a complexity of hybrid sex determination. Few valid inferences could be made regarding intraspecific sex determination from these hybrid data. Sex ratios from progeny testing of sex-reversed males (1∶3) and most sex-reversed females (1∶0) provide evidence for female heterogamety in O. aureus. Several aberrant ratios observed suggest Mendelian inheritance of an Autosomal Recessive Gene (F,f), epistatic to the major sex-determining Gene (W,Z). Sex ratios of triploids and gynogens support the hypothesis of recombination between the centromere and the major sex-determining locus. Progeny testing of a female mitogyne demonstrated the viability of a novel WW “superfemale”, which gave only female offspring. Not all data could be explained by a two-factor model of sex determination. Further exceptional sex ratios may be accounted for by rare Autosomal or environmental sex-modifying factors. It is concluded that O. aureus has a multifactorial mechanism of sex determination with the underlying primary mechanism of female heterogamety.

  • sex determination in the genus oreochromis 2 sex reversal hybridisation gynoGenesis and triploidy in o aureus steindachner
    Theoretical and Applied Genetics, 1991
    Co-Authors: G C Mair, A G Scott, D J Penman, D O F Skibinski, J A Beardmore
    Abstract:

    Sex ratios from 62 single-pair matings of normal broodstock O. aureus were highly heteroGeneous with an overall deficit of males (41.4%). Peaks in the sex ratio frequency distribution occurred at 1∶1, 3∶5 and 1∶3 (male∶female). Hybridisation of O. aureus with O. mossambicus, O. spilums and O. niloticus produced highly variable sex ratios, suggesting a complexity of hybrid sex determination. Few valid inferences could be made regarding intraspecific sex determination from these hybrid data. Sex ratios from progeny testing of sex-reversed males (1∶3) and most sex-reversed females (1∶0) provide evidence for female heterogamety in O. aureus. Several aberrant ratios observed suggest Mendelian inheritance of an Autosomal Recessive Gene (F,f), epistatic to the major sex-determining Gene (W,Z). Sex ratios of triploids and gynogens support the hypothesis of recombination between the centromere and the major sex-determining locus. Progeny testing of a female mitogyne demonstrated the viability of a novel WW "superfemale", which gave only female offspring. Not all data could be explained by a two-factor model of sex determination. Further exceptional sex ratios may be accounted for by rare Autosomal or environmental sex-modifying factors. It is concluded that O. aureus has a multifactorial mechanism of sex determination with the underlying primary mechanism of female heterogamety.