Congenic mice reveal genetic epistasis and overlapping disease loci for autoimmune diabetes and listeriosis

Wang, Nancy; Elso, Colleen M.; Mackin, Leanne; Mannering, Stuart I.; Strugnell, Richard A.; Wijburg, Odilia L. C.; Brodnicki, Thomas C.

doi:10.1007/s00251-014-0782-5

Cited by 7 publications

(12 citation statements)

References 29 publications

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“…In addition to revealing a new resistance locus for mycoplasmosis, our congenic NOD mice have now colocalized two infectious disease resistance loci, Mpr2 and Listr2, to the same genomic interval as Idd14, an autoimmune diabetes locus (17,18). This was perhaps not unexpected.…”

Section: Figmentioning

confidence: 65%

“…Congenic NOD mice reveal a mycoplasmosis resistance locus. We previously generated and used congenic NOD mice that harbor different B6-derived intervals for Chr13 to confirm and localize Listr2, an L. monocytogenes resistance locus (17). We hypothesized that the same genomic interval for Listr2 may also affect resistance to infection with M. pulmonis.…”

Section: Resultsmentioning

confidence: 99%

“…There is also no correlation between resistance to M. pulmonis infection and the risk for developing diabetes in the mouse strains we tested. The two M. pulmonis-susceptible strains, NOD and R6, are susceptible and resistant to the development of autoimmune diabetes, respectively, whereas the two M. pulmonis-resistant strains, B6 and R8, are resistant and susceptible to the development of autoimmune diabetes, respectively (17). The propensity to develop autoimmune diabetes therefore does not have an effect on respiratory mycoplasmosis.…”

Section: Figmentioning

confidence: 98%

“…Genetic variation in Slc11a1, the gene underlying Idd5.2, confers protection against infection with Salmonella enterica but increases the risk of developing autoimmune diabetes (15,16). More recently, we have shown that B6 mice harbor a more diabetogenic allele than NOD mice in the Idd14 locus when bred onto the NOD genetic background (17,18). These congenic NOD mice, which harbor the B6-derived Chr13 interval for Idd14, not only were more susceptible to autoimmune diabetes but also were more resistant to infection with Listeria monocytogenes.…”

mentioning

confidence: 94%

“…These congenic NOD mice, which harbor the B6-derived Chr13 interval for Idd14, not only were more susceptible to autoimmune diabetes but also were more resistant to infection with Listeria monocytogenes. Although the underlying gene(s) has yet to be identified, these studies colocalized Idd14 and Listr2, a resistance locus for listeriosis, to the same genomic interval on Chr13 (17,19).…”

mentioning

confidence: 99%

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Autoimmune-Disease-Prone NOD Mice Help To Reveal a New Genetic Locus for Reducing Pulmonary Disease Caused by Mycoplasma pulmonis

et al. 2018

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Mycoplasmas are bacterial pathogens of a range of animals, including humans, and are a common cause of respiratory disease. However, the host genetic factors that affect resistance to infection or regulate the resulting pulmonary inflammation are not well defined. We and others have previously demonstrated that nonobese diabetic (NOD) mice can be used to investigate disease loci that affect bacterial infection and autoimmune diabetes. Here we show that NOD mice are more susceptible than C57BL/6 (B6) mice to infection with , a natural model of pulmonary mycoplasmosis. The lungs of infected NOD mice had higher loads of and more severe inflammatory lesions. Moreover, congenic NOD mice that harbored different B6-derived chromosomal intervals enabled identification and localization of a new mycoplasmosis locus, termed , on chromosome 13. These congenic NOD mice demonstrated that the B6 allele for reduced the severity of pulmonary inflammation caused by infection with and that this was associated with altered cytokine and chemokine concentrations in the infected lungs. also colocalizes to the same genomic interval as and, genetic loci linked to listeriosis resistance and autoimmune diabetes susceptibility, respectively, suggesting that allelic variation within these loci may affect the development of both infectious and autoimmune disease.

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Section: Figmentioning

confidence: 65%

Section: Resultsmentioning

confidence: 99%

Section: Figmentioning

confidence: 98%

mentioning

confidence: 94%

mentioning

confidence: 99%

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Autoimmune-Disease-Prone NOD Mice Help To Reveal a New Genetic Locus for Reducing Pulmonary Disease Caused by Mycoplasma pulmonis

et al. 2018

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Evidence of genetic epistasis in autoimmune diabetes susceptibility revealed by mouse congenic sublines

Collin

Dugas

Pelletier³

et al. 2021

Immunogenetics

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Susceptibility to autoimmune diabetes is a complex genetic trait. Linkage analyses exploiting the NOD mouse, which spontaneously develops autoimmune diabetes, has proved to be a useful tool for the characterization of some of these traits. In a linkage analysis using 3A9 TCR transgenic mice on both B10.BR and NOD.H2 k backgrounds, we previously determined that both the Idd2 and Idd13 loci were linked to the proportion of immunoregulatory CD4 -CD8double negative (DN) T cells. In addition to Idd2 and Idd13, five other loci showed weak linkage to the proportion of DN T cells. Of interest, in an interim analysis, a locus on chromosome 12 is linked to DN T cell proportion in both the spleen and the lymph nodes. To determine the impact of this locus on DN T cells, we generated two congenic sublines, which we named Chr12P and Chr12D for proximal and distal, respectively. While 3A9 TCR:insHEL NOD.H2 k -Chr12D mice were protected from diabetes, 3A9 TCR:insHEL NOD.H2 k -Chr12P showed an increase in diabetes incidence. Yet, the proportion of DN T cells was similar to the parental 3A9 TCR NOD.H2 k strain for both of these congenic sublines. A genome-wide two dimensional LOD score analysis reveals genetic epistasis between chromosome 12 and the Idd13 locus. Altogether, this study identified further complex genetic interactions in defining the proportion of DN T cells, along with evidence of genetic epistasis within a locus on chromosome 12 influencing autoimmune susceptibility.

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Autoimmunity and antibody affinity maturation are modulated by genetic variants on mouse chromosome 12

Collin

Dugas

Chabot‐Roy

et al. 2015

Journal of Autoimmunity

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Congenic mice reveal genetic epistasis and overlapping disease loci for autoimmune diabetes and listeriosis

Cited by 7 publications

References 29 publications

Autoimmune-Disease-Prone NOD Mice Help To Reveal a New Genetic Locus for Reducing Pulmonary Disease Caused by Mycoplasma pulmonis

Autoimmune-Disease-Prone NOD Mice Help To Reveal a New Genetic Locus for Reducing Pulmonary Disease Caused by Mycoplasma pulmonis

Evidence of genetic epistasis in autoimmune diabetes susceptibility revealed by mouse congenic sublines

Autoimmunity and antibody affinity maturation are modulated by genetic variants on mouse chromosome 12

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