Sidman C L, Marshall J D, Beamer W G, Nadeau J H, Unanue E R
J Exp Med. 1986 Jan 1;163(1):116-28. doi: 10.1084/jem.163.1.116.
B lymphocytes from DBA/2Ha mice have a genetic defect characterized by a failure to differentiate into antibody-secreting cells in response to a family of lymphokines termed B cell maturation factors (BMFs). By contrast, B cells from DBA/2Ha mice respond normally in PFC assays to the B cell mitogen LPS, and macrophages from these mice are activated by one of the three BMFs. Two loci are responsible for the B cell defect in DBA/2Ha mice. One locus (Bmfr-1) is constitutively expressed throughout life, and maps approximately 13 cM distal to the brown locus on chromosome 4. A second locus (Bmfr-2) becomes active only after sexual maturity and is closely linked to the dilute locus on chromosome 9. At both loci, alleles determining responsiveness to BMFs are dominant over nonresponder alleles. The effect of Bmfr-2 on B cell responsiveness may be related to levels of the steroid sex hormones. DBA/2Ha mice offer a tool for studying the genetic and hormonal regulation of the immune system.
来自DBA/2Ha小鼠的B淋巴细胞存在一种遗传缺陷，其特征是在对一类称为B细胞成熟因子（BMF）的淋巴因子作出反应时无法分化为抗体分泌细胞。相比之下，来自DBA/2Ha小鼠的B细胞在PFC试验中对B细胞有丝分裂原LPS反应正常，并且这些小鼠的巨噬细胞可被三种BMF之一激活。两个基因座导致DBA/2Ha小鼠的B细胞缺陷。一个基因座（Bmfr-1）在整个生命过程中持续表达，定位在4号染色体上棕色基因座远端约13 cM处。第二个基因座（Bmfr-2）仅在性成熟后才活跃，并且与9号染色体上的稀释基因座紧密连锁。在这两个基因座上，决定对BMF反应性的等位基因对无反应等位基因呈显性。Bmfr-2对B细胞反应性的影响可能与类固醇性激素的水平有关。DBA/2Ha小鼠为研究免疫系统的遗传和激素调节提供了一种工具。
