Mhcii 1 ad

All animals used at the onset of the experiments were 8–10 week old male mice of the BALB/c background. BALB/c wt and CByJ.PL(B6)-Thy1a/ScrJ (thy1.1) mice were purchased from Jackson Laboratories (Bar Harbor, ME). Hemophilia A mice with a deletion in exon 16 of the F8 gene (BALB/c F8e16^−/−) were provided by Dr. David Lillicrap (Queens, Ontario, Canada). Hemophilia B mice with a targeted deletion of the promoter and the first 3 exons of the F9 gene had been backcrossed onto a BALB/c background for >10 generations.^{47 (link)} DO11.10-tg Rag2^−/− mice with a T cell receptor specific for a 323–339 of chicken OVA, presented by MHCII I-Ad, were originally obtained from Taconic (Hudson, NY). BALB/c mice with reporter gene knocked-in at FoxP3 locus (FoxP3-IRES-eGFP) were as previously described and kindly provided by Dr. Talal Chatila.^{48 (link)} Hemophilia B mice with GFP expression in FoxP3⁺ cells were generated by crossing BALB/c F9^−/− mice with FoxP3-IRES-eGFP BALB/c mice. Approximately 1 of 10 offspring showed the crossover event necessary to generate the F9 knock-out/FoxP3-GFP knock-in genotype (both genes are located on the X chromosome).^{7 (link)} Subsequent breeding generated homozygous females and hemizygous males. Animals were housed under special pathogen-free conditions at the University of Florida and treated under Institutional Animal Care and Use Committee-approved protocols.