Figure 3
Figure 3. Characterization of splenic B-cell subsets in fetal liver hematopoietic chimeras reveals an absolute dosage-dependent requirement for Maml1 in MZB development. (A) Representative contour plots showing that MZB precursors (MZP B) and MZB populations were absent in Maml1−/− fetal liver chimera, while reduced to about half of normal in Maml1+/− fetal liver chimera compared with the wild-type controls. Host-derived CD45.1+ cells were excluded from the analysis. (B) Compilation of data collected from all the fetal liver chimeras that were analyzed (Maml1+/+, n = 9; Maml1+/−, n = 21; Maml1−/−, n = 9). MZB cells were essentially absent in Maml1−/− chimeras and decreased in numbers in Maml1+/− heterozygous chimeras. Differences were highly statistically significant (P < .01; Student t test).

Characterization of splenic B-cell subsets in fetal liver hematopoietic chimeras reveals an absolute dosage-dependent requirement for Maml1 in MZB development. (A) Representative contour plots showing that MZB precursors (MZP B) and MZB populations were absent in Maml1−/− fetal liver chimera, while reduced to about half of normal in Maml1+/− fetal liver chimera compared with the wild-type controls. Host-derived CD45.1+ cells were excluded from the analysis. (B) Compilation of data collected from all the fetal liver chimeras that were analyzed (Maml1+/+, n = 9; Maml1+/−, n = 21; Maml1−/−, n = 9). MZB cells were essentially absent in Maml1−/− chimeras and decreased in numbers in Maml1+/− heterozygous chimeras. Differences were highly statistically significant (P < .01; Student t test).

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