Homozygous mice are viable and fertile with normal T and B cell development. These "Foxp3EGFP" mice co-express EGFP and the regulatory T cell-specific transcription factor Foxp3 under the control of the endogenous promoter. EGFP expression accurately identifies the Foxp3+ T cell population (more than 97% of Foxp3+ T cells were EGFP+), and Foxp3 mRNA expression strictly segregates with EGFP+ T cells. Due to X-inactivation in females, when the reporter construct in a heterozygous not a homozygous state, the number of EGFP+CD4+ T cells found in the peripheral blood of heterozygous females was approximately half that of hemizygote males. CD4+EGFP+ cells also exhibit normal regulatory T cell suppression of effector cell proliferation (following stimulation with anti-CD3 and anti-CD28 monclonal antibodies ). Some EGFP expression is noted in a small population of CD8+ thymocytes. These mutant mice may be useful in immunological studies, including studies of regulatory T cell proliferation, localization, and antigen independence during the primary immune response. On the congenic NOD background these mutant mice exhibit a diabetes incidence similar to NOD inbred mice.
This strain targets the GFP cassette downstream of the endogenous Foxp3 STOP codon with no defects in Foxp3 or regulatory T cell function observed.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This allele was originally published on a BALB/c genetic background (see Stock No. 006769). It should be noted that the phenotype could vary from that originally described. The strain description will be modified as published results become available.
