Fig. 8: Actively mutated MYD88 cooperate with Nfkbie deficiency in B cell. | Blood Cancer Journal

Fig. 8: Actively mutated MYD88 cooperate with Nfkbie deficiency in B cell.

From: Nfkbie-deficiency leads to increased susceptibility to develop B-cell lymphoproliferative disorders in aged mice

Fig. 8

a Scheme for retrovirally introducing wild type (WT) and mutant MYD88 (L265P) into activated Nfkbie+/+ and Nfkbie−/− mature splenic B cells. B cells were activated by anti-IgM with anti-CD40 for 24 h. They were then infected with a retrovirus expressing MYD88WT-GFP or MYD88L265P-GFP, and cultured with anti-CD40 for 36 h. Afterward, cells were washed to withdraw anti-CD40 (time (T) 0) and GFP-positive-cell percentages b and absolute numbers c were monitored at 48 h and 72 h. b Percentages of GFP-positive cells normalized to T0. Results are mean ± SD of three independent experiments performed in duplicate. c Fold changes of absolute cell numbers of GFP-positive cells normalized to T0. Data are mean ± SD of three independent experiments performed in duplicate. d Representative flow cytometry analysis of lymph node from CpG-injected mice of the indicated genotypes. Gates depict germinal center (GC) B cells (B220+CD19+CD95(Fas)+GL7+). The percentage of GC B cells and their cell number in the lymph node are shown. Each symbol represents one mouse (n = 3). Data are mean ± SEM. *p < 0.05.

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