Detection of a Large RIII-Derived Chromosomal Segment on Chromosome 10 in the H-2 Congenic Strain B10.RIII(71NS)/Sn

Dong, Penny; Hood, Leroy; McIndoe, Richard A.

doi:10.1006/geno.1996.0047

Cited by 8 publications

(5 citation statements)

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“…Analysis of the genome‐wide typing of these crosses identified not only the RIII‐derived fragment on chromosome 17, containing the MHC region, but also a large fragment on chromosome 10. This finding in fact confirmed a report from Dong et al 11 identifying the same fragment in B10.RIII/J mice derived from Jackson Laboratories, indicating that the fragment is a remnant from the original establishment of the congenic strain. B10.Q is another congenic mouse strain derived from a cross between the donor strain DBA/1 (H‐2 q ) and the background strain C57BL/10Sn(H‐2 b ), followed by several subsequent backcrosses to the background strain.…”

Section: Introductionsupporting

confidence: 89%

A genetic contamination in MHC‐congenic mouse strains reveals a locus on chromosome 10 that determines autoimmunity and arthritis susceptibility

Nandakumar

Holmdahl

2005

Eur J Immunol

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Among the arthritis-susceptible MHC (H-2)-congenic mouse strains, B10.RIII mice are highly susceptible to collagen-induced arthritis. Surprisingly, the B10.RIII strain was also more susceptible to the T cell independent model CAIA (collagen-antibody-induced arthritis). Through genome-wide genotyping, we found that the B10.RIII and B10.Q strains differed not only in chromosome 17 (MHC) but also in a region on chromosome 10, which contained a fragment from the MHC donor RIIIS/J. We isolated the chromosome 10 as well as the chromosome 17 segments on the B10.RIII and B10.Q backgrounds. Congenic mice containing the RIIIS/J-derived chromosome 10 segment showed significantly higher susceptibility and severity of arthritis with an enhanced autoimmune response to type II collagen. Furthermore, this chromosomal segment significantly promoted CAIA. Similarly, the RIIIS/J segment in chromosome 17 also promoted CAIA independently of other gene segments. These data show that other gene regions, apart from MHC class II, may explain effects both at the priming and effector level of arthritis observed in widely used MHC congenic strains. These new congenic fragments, on both chromosome 10 and 17, provide new mouse strains suitable for studies aiming at positional cloning of new genes associated with arthritis.

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Section: Introductionsupporting

confidence: 89%

A genetic contamination in MHC‐congenic mouse strains reveals a locus on chromosome 10 that determines autoimmunity and arthritis susceptibility

Nandakumar

Holmdahl

2005

Eur J Immunol

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“…Although we do not know of genetic contamination in the other MHC-congenic strains, the B10.RIII (H2 r ) strain contains a large MHC-donor RIII-derived region on chromosome 10 that correlates with increased susceptibility to models of arthritis, independent of the MHC locus (27, 28). To test whether this genetic contamination was responsible for the observed high frequency of IFNγ production by B10.RIII NK cells, we crossed B10.RIII mice with C57BL/6 mice to produce F 2 hybrid mice that were homozygous for RIII-derived genetic segments on either chromosome 10 or at the MHC locus.…”

Section: Resultsmentioning

confidence: 99%

Effects of MHC Class I Alleles on Licensing of Ly49A+ NK Cells

Jonsson

Yang

Kim

et al. 2010

The Journal of Immunology

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“…25 The possibility that Idd10, Idd17 and Idd18 represents the same genes as Cia5, Cia21 and Cia22 still remains, but the effects are dependent on genes either in the MHC region or on chromosome 10, which are the only (known) regions that differs between the B10.RIII and B10.Q strains. 26 Although mapping of susceptibility loci for complex diseases implies substantial work, we think it is important to identify naturally occurring allelic variants causing disease. They are likely to represent evolutionary selected alleles causing common diseases like RA in the 'wrong' genetic context and environment.…”

Section: Discussionmentioning

confidence: 99%

Identification of epistasis through a partial advanced intercross reveals three arthritis loci within the Cia5 QTL in mice

et al. 2005

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Identification of genes controlling complex diseases has proven to be difficult; however, animal models may pave the way to determine how low penetrant genes interact to promote disease development. We have dissected the Cia5/Eae3 susceptibility locus on mouse chromosome 3 previously identified to control disease in experimental models of multiple sclerosis and rheumatoid arthritis. Congenic strains showed significant but small effects on severity of both diseases. To improve the penetrance, we have now used a new strategy that defines the genetic interactions. The QTL interacted with another locus on chromosome 15 and a partial advanced intercross breeding of the two congenic strains for eight generations accumulated enough statistical power to identify interactions with several loci on chromosome 15. Thereby, three separate loci within the original QTL could be identified; Cia5 affected the onset of arthritis by an additive interaction with Cia31 on chromosome 15, whereas the Cia21 and Cia22 affected severity during the chronic phase of the disease through an epistatic interaction with Cia32 on chromosome 15. The definition of genetic interactions was a prerequisite to dissect the Cia5 QTL and we suggest the partial advanced intercross strategy to be helpful also for dissecting other QTL controlling complex phenotypes.

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Detection of a Large RIII-Derived Chromosomal Segment on Chromosome 10 in the H-2 Congenic Strain B10.RIII(71NS)/Sn

Cited by 8 publications

References 0 publications

A genetic contamination in MHC‐congenic mouse strains reveals a locus on chromosome 10 that determines autoimmunity and arthritis susceptibility

A genetic contamination in MHC‐congenic mouse strains reveals a locus on chromosome 10 that determines autoimmunity and arthritis susceptibility

Effects of MHC Class I Alleles on Licensing of Ly49A+ NK Cells

Identification of epistasis through a partial advanced intercross reveals three arthritis loci within the Cia5 QTL in mice

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