Balb c h 2d

B6.Ly5.1 (H2^b Ly5.1⁺) or BALB/c (H2^d) were purchased from Jackson and 129Sv (H2^b Ly5.2⁺) or TAP2^−/−β₂m^−/− mice were purchased from Taconic. All mice were used at the age of 8–12 weeks. LRBA^−/− mice were derived via blastocyst injection of embryonic stem cells harboring a gene-trap retrovirus42 (link) whose integration in the LRBA gene inactivates its expression by introduction of an artificial exon that terminates endogenous LRBA transcription and splicing to downstream exons. Southern blotting was used to identify murine progeny with significant transmission of the LRBA gene-trap integration and these chimeric mice were then crossed to 129Sv partners to obtain mice that have germline transmission of the LRBA mutant allele on a pure 129Sv genetic background. These LRBA^+/− progeny were then intercrossed to obtain LRBA-null homozygous mice with confirmation of the null homozygous genotype by a multiplex PCR. Northern blotting of kidneys and brains, two tissues that have abundant LRBA expression, confirmed that LRBA-null mice lack detectable mRNA expression from the LRBA locus. All animal experiments were approved by Institutional Animal Care and Use Committee (IACUC) of SUNY Upstate Medical University and performed in accordance with approved guidelines.