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. 2008 Aug 8;20(10):1279–1287. doi: 10.1093/intimm/dxn087

Fig. 1.

Fig. 1.

Primary B cell development in Fas-deficient HKI65 and HKIR mice. (A) Splenocytes were isolated from Fas-sufficient and Fas-deficient HKI65 and HKIR hemizygous mice as well as B6 mice and were stained with anti-B220 and anti-IgMa and anti-IgMb allotypic mAbs and analyzed by flow cytometry. HKI knock-in loci encode the IgMa allotype. The data shown are from pooled cells from two mice of each genotype. (B) Splenocytes from mice of the indicated genotypes were stained with anti-B220, anti-CD21 and anti-CD23 and analyzed by flow cytometry. Follicular (CD23high CD21low) and marginal zone (CD23low CD21high) sub-populations are gated. The data shown are representative of at least three independent experiments. (C) Splenocytes from mice of the indicated genotypes were stained with anti-B220, anti-IgD and anti-clonotypic E4 mAbs and analyzed by flow cytometry. All data shown in this figure are from cells in the B220+ gate. The results are representative of at least three independent experiments.