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beta2M0/N

eagle-i ID

http://harvard.eagle-i.net/i/0000012a-25bf-7988-f5ed-943080000008

Resource Type

  1. Mus musculus

Properties

  1. Resource Description
    Development: The beta2Mo mutant strain was generated by a targeted disruption of the beta2M gene into129-derived E14TG2a ES cell line (Koller BH et al, 1990). The NOD/LtJ strain was produced by backcrossing the mutation 10 times to NOD/LtJ inbred mice (Christianson et al, 1996). The line is currently at the >12th backcross generation on NOD/LtJ. The elimination of cell surface MHC class I expression blocks both insulitis and autoimmune diabetes in NOD/Lt mice (Katz J et al, 1993; Wicker et al, 1994; Wang et al, 1996).
  2. Related Disease
    type 1 diabetes mellitus
  3. Related Publication or Documentation
    Normal development of mice deficient in beta 2M, MHC class I proteins, and CD8+ T cells.
  4. Related Publication or Documentation
    beta2-microglobulin dependence of the lupus-like autoimmune syndrome of MRL-lpr mice.
  5. Related Publication or Documentation
    Major histocompatibility complex class I molecules are required for the development of insulitis in non-obese diabetic mice.
  6. Related Publication or Documentation
    The role of CD8+ T cells in the initiation of insulin-dependent diabetes mellitus.
  7. Related Publication or Documentation
    Resistance alleles at two non-major histocompatibility complex-linked insulin-dependent diabetes loci on chromosome 3, Idd3 and Idd10, protect nonobese diabetic mice from diabetes.
  8. Parental Strain Name
    NOD
  9. Genetic Alteration(s)
    Beta-2 microglobulin deletion
  10. Clinical or Environmental Source
    Controlled facility at Jackson labs
  11. Phenotype Findings
    Mice homozygous for the beta2M targeted mutation have little if any MHC class I protein expression on the cell surface.
  12. Phenotype Findings
    Immune responses involving CD8+ T-cells are severely deficient.
  13. Phenotype Findings
    Few CD8+ cytotoxic T-cells.
  14. Phenotype Findings
    Under some circumstances a compensatory increase in CD4+ cytotoxic T-cells.
  15. Location
    Genetically Modified NOD Mouse Core Facility (HMS)
 
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