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. 2015 Jan 20;125(12):1910–1921. doi: 10.1182/blood-2014-08-594655

Figure 4.

Figure 4

Defects in B-lymphoid cell development in Moz+/− mice are intrinsic to the hematopoietic system. (A) Experimental design. (B) Chimerism levels in recipient mice of Moz+/− or WT BM cells 4 months after transplantation. (C) Weights of spleen and thymus in recipient mice 4 months after transplantation. (D) Cellularity of spleen, thymus, and femurs (nucleated cells only). (E) Numbers of HSCs and early progenitors in the BM of recipient mice. Right panels show representative flow cytometry plots of the LSK population. (F) Enumeration of B-cell progenitors and mature B cells in the BM of recipient mice. The proportion of BM B lymphocytes in recipient mice is represented in the right panels. (G) Quantification of B-lymphoid cell subsets in the spleens of recipient mice. (H) Quantification of B cells in the peripheral blood of recipient mice. The proportion of B lymphocytes in the peripheral blood of recipient mice is represented in the right panels. Data above are presented as mean ± SEM (n = 6 donors and 18 recipients per genotype). Asterisks indicate a statistically significant difference between recipients of Moz+/− and WT BM at *P < .05, **P < .01, and ***P < .001. Cell surface markers used to discriminate between cell populations are outlined in supplemental Table 9. APC, allophycocyanin.