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. Author manuscript; available in PMC: 2020 Jul 15.
Published in final edited form as: J Immunol. 2019 Jun 5;203(2):418–428. doi: 10.4049/jimmunol.1900175

Figure 5. Development of B1–8i NP+ Igλ1+ but not NP+ Igλ2+ B-2 cells is disfavored in competition with an unrestricted BCR repertoire.

Figure 5

(A) Representative gating of NP+ Igλ1+, NP+ Igλ2+, bulk B1–8, WT, and residual host Fo B cells (CD23+CD93−) in bone marrow chimeras with CD45.1/2 B1–8i and CD45.2/2 WT donors in lethally-irradiated CD45.1/1 hosts.

(B-E) Percentage of NP+ Igλ1+ (B), NP+ Igλ2+ (C), bulk B1–8 (D), and WT (E) cells, normalized to B220+ cells, in splenic compartment. (T1 = CD23−CD93+, T2/3 = CD23+CD93+, Fo = CD23+CD93−, MZ = CD21hi CD23lo). Statistics were calculated for n = 5 chimeric mice, and one-way ANOVA with Dunnett’s multiple comparisons test was used to compare T2/3, Fo, and MZ populations to the T1 reference population and calculate p-values.

(F-G) Nur77-eGFP expression in Fo (G) and MZ (H) B cells from B1–8:WT chimeras described in (A). n = 4 mice were used to calculate Nur77-eGFP MFI and one-way ANOVA with Tukey’s multiple comparisons test was used to calculate p-values.

**p<0.01, ***p<0.001, ****p< 0.0001.