Abstract
The genesis and maturation of murine B lymphocytes in the bone marrow is marked by the sequential appearance of the B-220 molecule, cytoplasmic u chains, surface IgM and IgD [1, 2]. In the spleen at least three distinct populations of B cells can be identified on the basis of the relative concentrations of surface IgM and IgD [3]. One of these, carrying high IgD and low IgM concentrations, is absent in CBA/N mice, which are homozygous for the X-linked immunodeficiency (xid) trait [3]. Transplantation of normal bone marrow or foetal liver cells into CBA/N mice results in normal B cell development, implying that the xid defect is intrinsic to the cells and not microenvironmental [4]. Splenic B lymphocytes in female xid/+ heterozygotes were recently found to express mainly the non-xid carrying chromosome in a population associated with IgG3 production [4]: presumably those stem cells in which the xid-carrying X-chromosome was active showed at least a partial failure to differentiate into B lymphocytes. Thus, the defect appeared to act directly on B cells rather than on some other cell type influencing B cell development.
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© 1985 Plenum Press New York
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Witkowski, J., Forrester, L.M., Ansell, J.D., Micklem, H.S. (1985). Influence of the XID Mutation on B Lymphocyte Development in Adult Mice. In: Klaus, G.G.B. (eds) Microenvironments in the Lymphoid System. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2463-8_6
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DOI: https://doi.org/10.1007/978-1-4613-2463-8_6
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