Development of B lymphocytes in mice heterozygous for the X-linked immunodeficiency (xid) mutation. xid inhibits development of all splenic and lymph node B cells at a stage subsequent to their initial formation in bone marrow.
CBA/N mice were crossed with CBA/Ca-Pgk-1a to produce female F1 hybrids that were heterozygous for both xid and the phosphoglycerate kinase 1 (PGK-1) allozymes. PGK acted as a quantifiable marker for the frequency of cells in which the xid-bearing X chromosome was active in lymphocytic and other cell populations. In adults, such cells (termed xid cells) were virtually absent in FACS-sorted splenic and lymph node B cells, and in all three splenic subpopulations distinguished on the basis of their relative expression of membrane mu and delta chains. Thus, the xid mutation appeared to compromise the development of all B cells. Erythrocytes, thymocytes, T cells, and granulocytes were unaffected. Selection against xid cells was less pronounced in the spleens of 2-6-wk-old mice. In the bone marrow, there was evidence for selection against xid in the production of B cells (except at 2 wk of age), but not at the pre-B cell level. These data suggest that, in competition with normal non-xid cells, newly-formed xid B cells were less likely to be incorporated into the peripheral B cell pool.
D000818:Animals; D001402:B-Lymphocytes / Q000473:pathology*; D001853:Bone Marrow / Q000473:pathology; D002454:Cell Differentiation; D004303:Dosage Compensation, Genetic; D004912:Erythrocytes / Q000201:enzymology; D005260:Female; D005819:Genetic Markers; D006412:Hematopoietic Stem Cells / Q000473:pathology*; D006579:Heterozygote; D007153:Immunologic Deficiency Syndromes / Q000235:genetics / Q000473:pathology*; D008198:Lymph Nodes / Q000473:pathology; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D008817:Mice, Mutant Strains / Q000276:immunology*; D010735:Phosphoglycerate Kinase / Q000097:blood / Q000235:genetics; D013154:Spleen / Q000473:pathology
D005819:Genetic Markers; D010735:Phosphoglycerate Kinase