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. Author manuscript; available in PMC: 2020 Aug 17.
Published in final edited form as: Nat Immunol. 2020 Feb 17;21(3):331–342. doi: 10.1038/s41590-020-0598-4

Fig. 5. GCBCs are sensitive to dual mitochondrial and peroxisomal FAO in vitro and in vivo.

Fig. 5.

a, Tabulated cell death data, measured by flow cytometry as fixable viability stain (FVS) and Caspglow™ positive, from in vitro activated or d13 GCBCs cultured with anti-CD40 in the presence of the indicated inhibitors for the indicated times (n=4). b, Cell cycle analysis of cells treated as in (a) pulsed with 25 μM EdU for 30min prior to harvest (n=4). c, d and e, Absolute number of live splenic NP-specific GCBCs (c), naïve NP− B cells (d) and MFI of 2-NBDG of GCBCs after 30min 2-NBDG in vitro pulse (e) from mice at d14 post NP-CGG immunization given 22mg/kg etomoxir and 11mg/kg thioridazine or vehicle only at d9 and d13 post-immunization. (a) and (b) depict 1 representative of 2 experiments with 4 replicate cultures of indicated samples. GCBCs were pooled from 19 B1–8+/– Balb/c mice at day 14 after NP-CGG immunization and NBC were pooled from 6 unmanipulated B1–8+/– Balb/c mice to generate in vitro activated B cells. (c-d) are from one experiment with two inhibitor doses, which was replicated with an additional in vivo dose in Extended Data Fig. 5; Bars represent mean +/− SEM; *p ≤ 0.05; ***p ≤ 0.001, **** p ≤ 0.0001 by unpaired, two-tailed t-test.