• H2-Ab1 gene is a mouse gene that encodes the β chain of an MHC class II molecule, playing a crucial role in antigen presentation and CD4+ T cell activation. H2-Ab1 is expressed in various tissues, including the spleen, liver, and lungs.
• In B-BM12 mice, three discontinuous base mutations occurred at exon 2 of the H2-Ab1 gene, resulting in the substitution of three amino acids: isoleucine (Ile, I) at position 94 was replaced by phenylalanine (Phe, F), arginine (Arg, R) at position 97 was replaced by glutamine (Gln, Q), and threonine (Thr, T) at position 98 was replaced by lysine (Lys, K).
• H2-Ab1 mRNA was detectable in spleen and lung of wild-type C57BL/6JNifdc mice and homozygous B-BM12 mice, and the point mutation was confirmed via Sanger sequencing.
• B-BM12 mice mouse model, with its specific point mutations in MHC class II molecules, is mainly used to artificially induce autoimmune disease models such as systemic lupus erythematosus and dry eye, as well as to study chronic transplant rejection mediated by CD4+ T cells in skin transplantation.

Gene targeting strategy for B-BM12 mice. In B-BM12 mice, three discontinuous base mutations occurred at exon 2 of the H2-Ab1 gene, resulting in the substitution of three amino acids: isoleucine (Ile, I) at position 94 was replaced by phenylalanine (Phe, F), arginine (Arg, R) at position 97 was replaced by glutamine (Gln, Q), and threonine (Thr, T) at position 98 was replaced by lysine (Lys, K).

Strain specific analysis of H2-Ab1 mRNA expression in wild-type C57BL/6JNifdc mice and B-BM12 mice by RT-PCR. Spleen and lung RNA were isolated from wild-type C57BL/6JNifdc mice (+/+) and homozygous B-BM12 mice (Mut/Mut), then cDNA libraries were synthesized by reverse transcription, followed by PCR with H2-Ab1 primers. H2-Ab1 mRNA was detectable in wild-type C57BL/6JNifdc mice and homozygous B-BM12 mice, and the point mutation was confirmed via Sanger sequencing.