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CD40[0]/N

eagle-i ID

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

Resource Type

  1. Mus musculus

Properties

  1. Resource Description
    Development: The CD40 gene was disrupted by replacing exon 3 by the neomycin resistance gene (Kawabe et al, Kikutani H, 1994). Mice carrying the CD40 null mutation were transferred to the NOD background (Korganow AS et al, Mathis D, 1999). The line is currently at the >13th backcross to NOD/LtJ . Homozygous mutant mice show a deficiency in T cell activation. The mutation causes a significant reduction of CD23 expression on mature B cells and relatively decreased number of IgM bright and IgD dull B cells. The mutant mice mount IgM responses but no IgG, IgA, and IgE responses to thymus dependent antigens. However, IgG as well as IgM responses to thymus-independent antigens are normal (Kawabe et al, Kikutani H, 1994).
  2. Related Disease
    type 1 diabetes mellitus
  3. Related Publication or Documentation
    From systemic T cell self-reactivity to organ-specific autoimmune disease via immunoglobulins.
  4. Related Publication or Documentation
    The immune responses in CD40-deficient mice: impaired immunoglobulin class switching and germinal center formation.
  5. Parental Strain Name
    NOD
  6. Genetic Alteration(s)
    CD40 deletion
  7. Clinical or Environmental Source
    Controlled facility at Jackson labs
  8. Phenotype Findings
    Deficiency in T cell activation.
  9. Phenotype Findings
    The mutant mice mount IgM responses but no IgG, IgA, and IgE responses to thymus dependent antigens. IgG as well as IgM responses to thymus-independent antigens are normal.
  10. Phenotype Findings
    Homozygous CD400 mice on the NOD background are protected from diabetes.
  11. Location
    Genetically Modified NOD Mouse Core Facility (HMS)
 
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The eagle-i Consortium is supported by NIH Grant #5U24RR029825-02 / Copyright 2016