Baum C M, Macke K A, Nahm M H
Department of Microbiology and Immunology, Washington University School of Medicine, St. Louis, MO 63110.
Immunol Lett. 1987 Jul;15(3):179-85. doi: 10.1016/0165-2478(87)90022-8.
DBA/2Ha mice have an X-chromosome-linked immunodeficiency and lack the receptor to a TRF (T cell replacing factor) on a subpopulation of B cells. Their immunodeficiency is considered to resemble that of CBA/N, another X-chromosome-linked immunodeficiency. To facilitate direct comparisons of the two immunodeficiencies and to study the in vivo manifestations of DBA/2Ha immunodeficiency, we measured phenotypes and functions of B cells of DBA/2Ha mice. We found that the expression of sIgM among B cells is normal in DBA/2Ha mice, heterozygous females equally express both affected and normal B cell subpopulations, and DBA/2Ha mice respond well to a TI-2 antigen (TNP-Ficoll) and a polyclonal activator (LPS). Unlike CBA/N, DBA/2Ha mice demonstrate very little in vivo immunodeficiencies.
DBA/2Ha小鼠存在X染色体连锁免疫缺陷，且B细胞亚群缺乏TRF（T细胞替代因子）受体。它们的免疫缺陷被认为与另一种X染色体连锁免疫缺陷CBA/N相似。为便于对这两种免疫缺陷进行直接比较，并研究DBA/2Ha免疫缺陷的体内表现，我们检测了DBA/2Ha小鼠B细胞的表型和功能。我们发现，DBA/2Ha小鼠B细胞中sIgM的表达正常，杂合子雌性同样表达受影响和正常的B细胞亚群，并且DBA/2Ha小鼠对TI-2抗原（TNP-菲可）和多克隆激活剂（LPS）反应良好。与CBA/N不同，DBA/2Ha小鼠在体内表现出的免疫缺陷非常少。
