Physiology of B cells in mice with X-linked immunodeficiency (xid). III. Disappearance of xid B cells in double bone marrow chimeras.
Evidence is presented that B cells from mice with X-linked immunodeficiency (xid) differentiate at a slower rate than normal B cells. This conclusion stems from studies in which (B6 X CBA/J)F1 mice were heavily irradiated (1,000 rads) and reconstituted with a mixture of T-depleted marrow cells taken from (a) nondefective B6 mice (H-2b) and (b) xid CBA/N or nondefective CBA/Ca mice (both H-2k). With transfer of CBA/Ca plus B6 marrow cells, the irradiated recipients become repopulated with B cells derived from both parental marrow sources; except for an early imbalance (probably reflecting Hh resistance), the degree of chimerism remained relatively stable over a period of more than 6 months. Very different results occurred with transfer of a mixture of xid CBA/N and normal B6 marrow. Within the first 2 months after marrow reconstitution, a low but significant proportion of the B cells in both spleen and lymph nodes were of CBA/N origin. Thereafter the proportion of these cells fell progressively, and by 6-9 months virtually all of the B cells were of B6 origin. This gradual decline in CBA/N-derived cells did not apply to other cell types, i.e., T cells or pluripotential stem cells. Analogous results were obtained with transfer of CBA/N vs. CBA/Ca marrow cells into sublethally irradiated (750 rads) (CBA/N X DBA/2)F1 male vs. female mice. For example, CBA/N-marrow derived B cells differentiated effectively and survived for long periods in F1 male mice (xid----xid) but not in F1 female mice (xid----normal). The finding that xid B cells eventually disappear in the presence of normal B cells strengthens the view that xid B cells are an abnormal population not represented in normal mice.
D000818:Animals; D000921:Antibody-Producing Cells / Q000502:physiology; D001402:B-Lymphocytes / Q000502:physiology*; D001853:Bone Marrow / Q000276:immunology*; D016026:Bone Marrow Transplantation; D002470:Cell Survival; D005260:Female; D005362:Ficoll / Q000031:analogs & derivatives / Q000276:immunology; D006412:Hematopoietic Stem Cells / Q000502:physiology; D006462:Hemolytic Plaque Technique; D007153:Immunologic Deficiency Syndromes / Q000235:genetics / Q000276:immunology*; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA / Q000235:genetics*; D011828:Radiation Chimera; D013601:T-Lymphocytes / Q000502:physiology; D014301:Trinitrobenzenes / Q000276:immunology; D014960:X Chromosome
D008070:Lipopolysaccharides; C020529:TNP-ficoll; D014301:Trinitrobenzenes; D005362:Ficoll