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Strain Code 01C42 [CBA/NCr] (designated previously as CBA/HN)

Origin and Characteristics

To N 1966 from Harwell carrying gene for foam cell reticulosis as heterozygous stock. The mutant was found in a radiation experiment conducted with the CBA/CaH strain. sibmated since introduction to N.

Genetics

A, B, C, Xid
Agouti (wild type)
Genes:

Car-2a, Ce-2b, Es-1b, Es-3c, Es-10b, Gpd-1b, Gpi-1b, Gusb, Hbbd, Idh-1b, Lva, Mod-1b, Mup-1a, Pep-3b, Pgm-1b, Trfa
Hc1, H-2Dk, H-2Kk, Lyb-2b, Lyt-1a, Lyt-2a, Lyt-3b, Thy-1a, Tlab.

Diseases

Non-Neoplastic (Induced)

  • Lethal dose 50 of Salmonella typhimurium for CBA/N was 1000-fold less than for CBA/caHN; the increased susceptibility was X-linked from F1 studies. (514)
  • Plasmodium yoelii and Babesia microti infections were more severe and lasted longer in defective F1 males than in normal males. (334,313)

Other Characteristics

Immunologic

  • The CBA/N mouse carries an X-linked recessive defect expressed in B lymphocytes. (011,307)
  • Grafts of fetal liver from CBA/H-T6T6 into irradiated or unirradiated immunodeficient CBA/N mice indicated that CBA/N mice are deficient in a category of pre-B cells which are found in fetal liver. (532)
  • Most of the functional behavior of B cells can be explained by a deletion of a mature B cell subset. (491,637,533)
  • B lymphocytes in spleen are reduced in number. (636)
  • B cells with high IgD.IgM ratios are absent. (832)
  • B cells are Lyb 3-, Lyb 5-, and Lyb 7-. (104,001,717)
  • B cell surfaces have low Mls determinants and low C3 receptors. (491,001,634)
  • No antibody formed in response to rl.rC. (633)
  • B cells from male and female (CBA/N x CBA/CaJ)F1 were receptive to T cells help from female F1 T cells, but male T cells could not augment polyclonal B cell responses of either male or female F1 mice to LPS, suggesting an intrinsic T cell defect. (224)
  • B cells activated by both DNP-LPS and DNP-chicken gamma globulin are rendered tolerant by prior exposure to DNP-Ficoll, implying possession of a B cell type not found at any stage during ontogeny o normal mice. (443)
  • When DNP-hemocyanin is administered after DNP-MGG, B cells are unresponsive to subsequent challenge with DNP-hemocyanin, mimicking 3-5 day neonatal B cells. (459)
  • No anti-PC IgM or IgG antibodies produced against phosphorylcholine conjugated T-dependent or T-independent antigens, but IgE antibodies to PC-determinant produced when immunized with PC-keyhole limpet hemocyanin. (365)
  • Immature B cells wre functionally indistinguishable from normal immature cells, in that both could be triggered to respond to thymus-independent antigens, provided they were supplied with helper T cells, supporting the idea that the CBA/N B cells have deviated during development so that only thymus-dependent B cells develop. (414)
  • Fail to produce at least some seta of high affinity antibodies after immunization with sheep erythrocytes (SRBC). (307)
  • Primary IgM anti-SRBC response is 10-50% of normal, and primary IgG anti-SRBC response is less than 10% of normal. (635)
  • No response to DNP-lysyl-Ficoll, TNP-Ficoll, or TNP-dextran. (637,490,716)
  • IgM response to type III pneunococcal polysaccharide (LPS) was extremely low, and response to TNP-LPS was low. (011,560)
  • Male and femal x-linked responsiveness to Type III pneumococcal polysaccharide (SSS-III) differ. Both produce an extremely low antibody response to SSS-III but females tend to respond slightly better than males as measured by SSS-III specific PFC. (011)
  • Functional colony-forming B cells are entirely lacking. (360)
  • CBA/N mice have high natural killer cell activity as do other CBA sublines which do not have the X-linked defect. (624,625)
  • The X-linked defect of T-independent immune response was completely expressed in CBA/N x NZB mice, suggesting that the NZB B cell abnormality resulting in excessive IgM production occurs in the B cell population affected by the X-linked defect. (731)
  • Although the B-cell response to bromelain-treated mouse erythrocytes is under sex-linked control, low levels of anti-BrMRBC PFC were induced by either specific (17XL Plasmodium yoelii) or nonspecific mechanisms (LPS), and the defect was largely overcome with age in both homozygous and hemizygous mice, probably as a result of environmental stimulation. (597)
  • Response to SRBC and LPS increased markedly with age, and spleen cells showed a distinct age-related increase in the percentage of surface lg+ cells. (792)