Nonobese diabetic mouse congenic analysis reveals chromosome 11 locus contributing to diabetes susceptibility, macrophage STAT5 dysfunction, and granulocyte-macrophage colony-stimulating factor overproduction.

@article{Litherland2005NonobeseDM,
  title={Nonobese diabetic mouse congenic analysis reveals chromosome 11 locus contributing to diabetes susceptibility, macrophage STAT5 dysfunction, and granulocyte-macrophage colony-stimulating factor overproduction.},
  author={Sally A. Litherland and Kristie M. Grebe and Nicole S. Belkin and Edward Paek and Jessica Elf and Mark Atkinson and Laurence M Morel and Michael J Clare-Salzler and Marcia Mcduffie},
  journal={Journal of immunology},
  year={2005},
  volume={175 7},
  pages={4561-5}
}
Unstimulated monocytes of at-risk/type 1 diabetic humans and macrophages of the NOD mouse have markedly elevated autocrine GM-CSF production and persistent STAT5 phosphorylation. We analyzed the relationship between GM-CSF production and persistent STAT5 phosphorylation in NOD macrophages using reciprocal congenic mouse strains containing either diabetes-susceptible NOD (B6.NODC11), or diabetes-resistant C57L (NOD.LC11) loci on chromosome 11. These intervals contain the gene for GM-CSF (Csf2… CONTINUE READING

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The immunopathogenic roles of antigen presenting cells in the NOD mouse

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