The CBA/N subline expresses an X-linked immunological defect which appears to be confined to the bone marrow-derived (B) lymphocyte lineage ( 1, 2, 3, 4, 5, 6, 7, 8). Although the precise nature of the defect is poorly understood, the functional consequences suggest that a maturation arrest of B-lymphocyte development has taken place ( 9, 10).
The CBA/N subline (also known as CBA/HN mice in earlier publications) was derived from the CBA/Harwell line. In 1966, mice with the spontaneous mutation for foam cell reticulosis (fm+) were imported to the NIH. The fm mutation arose in offspring of two to three breeding pairs of CBA/H mice in 1963 and is a homozygous lethal autosomal recessive gene ( 11), CBA/N mice were derived from fm+/fm- heterozygotes by brother-sister mating of fm-/fm- offspring whose phenotype was confirmed by progeny testing. Only a small number of such mice were bred, and in 1968 the subline almost was lost save for one pregnant female. All subsequent CBA/N mice are derived from that one litter of six females and one male. By 1972, when a defect in IgM serum levels was first noted ( 1), the subline had undergone 20 generations of brother-sister mating.
The phenotypic abnormalities of the CBA/N subline are summarized in Table 1. Most, if not all, of their functional behavior can be explained by a deletion of a mature B-lymphocyte subset. These mice provide an interesting model for a restricted immunologic defect and for studying the regulation of B lymphocyte differentiation. They have allowed the definition of a set of alloantigens which are expressed only on a subset of normal B cells, namely, those which appear to be absent in the CBA/N strain ( 12, 13). The mice are available to interested investigators through the NIH.
1. Amsbaugh, D.F., Hansen, C.T., Prescott, B., Stashak, P.W., Barthold, D.R., and Baker, P.J. (1972). J. Exp. Med. 136: 931.
See also
PubMed.
2. Scher, I., Frantz, M.M., and Steinberg, A.D. (1973). J. Immunol. 110: 1396.
See also
PubMed.
3. Scher, I., Steinberg, A.D., Berning, A.K., and Paul, W.E. (1975). J. Exp. Med. 142: 637.
See also
MGI.
4. Scher, I., Ahmed, A., Steinberg, A.K., and Paul, W.E. (1975). J. Exp. Med. 141: 788.
See also
MGI.
5. Scher, I., Sharrow, S.O., Wistar, R., Jr., Asofsky, R., and Paul, W.E. (1976). J. Exp. Med. 144: 494.
See also
PubMed.
6. Cohen, P.L., Scher, I., and Mosier, D.E. (1976). J. Immunol. 116: 301.
See also
MGI.
7. Mosier, D.E., Scher, I., and Paul, W.E. (1976). J. Immunol. 117: 1363.
See also
PubMed.
8. Finkelman, F.D., Smith, A.H., Scher, I., and Paul, W.E. (1975). J. Exp. Med. 142: 1316.
See also
MGI
9. Kincade, P.W. (1977). J. Exp. Med. 145: 249.
See also
PubMed.
10. Mosier, D.E., Zitron, I.M., Mond, J.J., Ahmed, A., Scher, I., and Paul, W.E. (1977). Immunol. Rev. 37: 89.
See also
PubMed.
11. Lyon, M.F., Hulse, E.V., and Rowe, C.E. (1965). J. Med. Genet. 2: 99.
See also
MGI.
12. Ahmed, A., Scher, I., Sharrow, S.O., Smith, A.H., Paul, W.E., Sachs, D.H., and Sell, K. W. (1977). J. Exp. Med. 145: 101.
See also
MGI.
13. Huber, B., Gershon, R.K., and Cantor, H. (1977). J. Exp. Med. 145: 10.
See also
MGI.