Mice homozygous for the Cd4tm1Knw knock-out have a significant block in CD4+ T cell development and show a Class II restricted deficit in helper T cell activity and other T cell responses. These NOD Cd4-deficient mice have decreased susceptibility to autoimmune diabetes and thus are diabetes resistant.
Dr. David Serreze, The Jackson Laboratory
Genetic Background | Generation |
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|
Allele Type | Gene Symbol | Gene Name |
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Targeted (Null/Knockout) | Cd4 | CD4 antigen |
The initiation of autoimmune insulin-dependent diabetes mellitus (IDDM) in the NOD mouse model entails MHC class I-restricted CD8 T cell responses against pancreatic beta cell antigens. CD8 T cells require helper functions provided by MHC class II-restricted CD4 T cells to exert their full diabetogenic effects. Mice homozygous for the Cd4tm1Knw knock-out have a significant block in CD4+ T cell development and show a Class II restricted deficit in helper T cell activity and other T cell responses. These NOD Cd4-deficient mice, therefore, have decreased susceptibility to autoimmune diabetes and thus are diabetes resistant.
Allele Name | targeted mutation 1, Barbara B Knowles |
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Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | CD4-; CD4D |
Gene Symbol and Name | Cd4, CD4 antigen |
Gene Synonym(s) | |
Strain of Origin | 129S/SvEv-Gpi1c |
Chromosome | 6 |
Molecular Note | A neomycin resistance gene was inserted into exon 5. |
Mutations Made By | Dr. Barbara Knowles, Institute of Medical Biology |
When using the NOD.Cd4null mouse strain in a publication, please cite the originating article(s) and include JAX stock #003090 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Homozygous for Cd4<tm1Knw>, 1 pair minimum |
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