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BDC2.5/N Thy1.1

eagle-i ID


Resource Type

  1. Mus musculus


  1. Resource Description
    Development: The BDC2.5 TCR alpha and beta sequences were co-injected into (B6xSJL)F2 eggs. The integration site for these BDC2.5 TCR transgenes was localized to chromosome 13 near the D13mit125 marker (Katz et al , Mathis D. 1993). BDC2.5/N Thy1.1 mice are created by crossing BDC2.5/N with NOD.Thy1a (NOD.NON-Thy1a/1LtJ). Thy1.1 is an allogenic marker from PL/J back-crossed onto NOD. (Fabien N et al, Thivolet C. 1995). The BDC2.5/N Thy1.1 line is currently at the N22 F6 backcross generation. On the NOD background, mice carrying the transgenes have a reduced incidence of diabetes relative to NOD/LtJ controls (12% incidence at age 30 weeks). BDC2.5/N animals show a generalized and very extensive islet infiltration after a few weeks of age, but most remain free of overt diabetes for long periods or develop forms of insulitis that does not cause beta cells destruction. The BDC2.5/N Thy1.1 congenic strain carries the T lymphocyte specific Thy1a (Thy1.1) allele. Donor T cells can be easily distinguished from recipient T cells by both flow cytometric and histological analysis.
  2. Related Disease
    type 1 diabetes mellitus
  3. Related Publication or Documentation
    Major histocompatibility complex class I molecules are required for the development of insulitis in non-obese diabetic mice.
  4. Related Publication or Documentation
    Pancreatic lymph nodes are early targets of T cells during adoptive transfer of diabetes in NOD mice.
  5. Parental Strain Name
  6. Genetic Alteration(s)
    TCR alpha /beta, Thymus Cell Antigen 1a variant insertion
  7. Clinical or Environmental Source
    Controlled facility at Jackson labs
  8. Location
    Genetically Modified NOD Mouse Core Facility (HMS)
Provenance Metadata About This Resource Record

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