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BDC2.5/N Thy1.1

eagle-i ID

http://harvard.eagle-i.net/i/0000012a-25bf-7988-f5ed-94308000000f

Resource Type

  1. Mus musculus

Properties

  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
    NOD
  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)
 
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