X-Linked Immune Deficiency (xid) of CBA/N Mice

Abstract

The CBA/N mouse strain was bred at the National Institutes of Health from a single litter of a CBA/Harwell mouse. After more than 20 generations of brother-sister mating, the mice derived from this litter, which had normal vigor and reproductive capacity under laboratory conditions, were considered to be inbred. In the early 1970s, it was shown that these mice made abnormal immune responses to polysaccharide antigens (Amsbaugh et al. 1972; Scher et al. 1973). Studies of the inheritance of this unresponsiveness demonstrated that F1 male progeny of crosses between CBA/N females and immunologically normal male mice were unresponsive, whereas F1 female progeny were normal. Female and male progeny of crosses between CBA/N males and normal female mice that were heterozygous and hemizygous, respectively, for the X-chromosome of the responsive strain were responders. These data are consistent with an X-linked recessive gene (xid) controlling unresponsiveness (Table 1). Recent mapping studies have located the xid genes (or group of closely linked genes) between the tabby and hypophosphatemia genes on the X-chromosome (Berning et al. 1980). The large number of X-linked human immune deficiency diseases (Cooper and Seligmann 1977), the association of serum IgM levels with the number X-chromosomes of an individual (Adinolfi et al. 1978), and the existence of a second mouse strain (DBA/2Ha) with an X-linked immune abnormality (Tominaga et al. 1980) suggest that the X-chromosome bears many loci influencing immunity.