Genetic analysis of susceptibility to colitis in IL 10-deficient mice

Maehler, Michael; Most, Claudia; Schmidtke, Sybille; Hedrich, Hans Juergen

doi:10.1016/s0016-5085(08)80177-1

Cited by 2 publications

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“…The peak marker for Hbnr12 on proximal Mmu8 is between D8Mit64 and D8Mit205 where the two strains have different haplotypes for glutathione reductase. A QTL for susceptibility to cytokine deficiency colitis lies close by at 28 cM (Mähler et al 2002). Il15 at 84·8 Mb, is close to the peak of the more distal Hbnr11 (peak marker D8Mit195, 85·1 Mb).…”

Section: Discussionmentioning

confidence: 99%

Quantitative trait loci for resistance to Heligmosomoides bakeri and associated immunological and pathological traits in mice: comparison of loci on chromosomes 5, 8 and 11 in F2 and F6/7 inter-cross lines of mice

et al. 2009

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A comparison of F2 and F6/7 inter-cross lines of mice, derived from CBA and SWR parental strains, has provided strong evidence for several previously undetected quantitative trait loci (QTL) for resistance to Heligmosomoides bakeri. Five QTL affecting average faecal egg counts and/or worm burdens in week 6 were detected on mouse chromosomes 5 (Hbnr9 and Hbnr10), 8 (Hbnr11) and 11 (Hbnr13 and Hbnr14). Three QTL for faecal egg counts in weeks 4 and 6 were found on both chromosomes 5 (Hbnr9) and 11 (Hbnr13 and Hbnr14). Two QTL for the mucosal mast cell protease 1 (MCPT1) response were located on chromosomes 8 (Hbnr11) and 11 (Hbnr13), two for the IgG1 antibody response to adult worms on chromosomes 5 (Hbnr10) and 8 (Hbnr11), two for PCV in week 6 on chromosomes 5 (Hbnr9) and 11 (Hbnr13), and two for the granulomatous response on chromosome 8 (Hbnr12) and 11 (Hbnr15). Our data emphasize that the control of resistance to H. bakeri is multigenic, and regulated by genes within QTL regions that have a complex range of hierarchical relationships.

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Section: Discussionmentioning

confidence: 99%

Quantitative trait loci for resistance to Heligmosomoides bakeri and associated immunological and pathological traits in mice: comparison of loci on chromosomes 5, 8 and 11 in F2 and F6/7 inter-cross lines of mice

et al. 2009

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The Immunology of Mucosal Models of Inflammation

Strober

Fuss

Blumberg

2002

Annu. Rev. Immunol.

1,235

1,096

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In recent years the status of the inflammatory bowel diseases (IBDs) as canonical autoimmune diseases has risen steadily with the recognition that these diseases are, at their crux, abnormalities in mucosal responses to normally harmless antigens in the mucosal microflora and therefore responses to antigens that by their proximity and persistence are equivalent to self-antigens. This new paradigm is in no small measure traceable to the advent of multiple models of mucosal inflammation whose very existence is indicative of the fact that many types of immune imbalance can lead to loss of tolerance for mucosal antigens and thus inflammation centered in the gastrointestinal tract. We analyze the immunology of the IBDs through the lens of the murine models, first by drawing attention to their common features and then by considering individual models at a level of detail necessary to reveal their individual capacities to provide insight into IBD pathogenesis. What emerges is that murine models of mucosal inflammation have given us a road map that allows us to begin to define the immunology of the IBDs in all its complexity and to find unexpected ways to treat these diseases.

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Genetic analysis of susceptibility to colitis in IL 10-deficient mice

Cited by 2 publications

References 0 publications

Quantitative trait loci for resistance to Heligmosomoides bakeri and associated immunological and pathological traits in mice: comparison of loci on chromosomes 5, 8 and 11 in F2 and F6/7 inter-cross lines of mice

Quantitative trait loci for resistance to Heligmosomoides bakeri and associated immunological and pathological traits in mice: comparison of loci on chromosomes 5, 8 and 11 in F2 and F6/7 inter-cross lines of mice

The Immunology of Mucosal Models of Inflammation

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