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. Author manuscript; available in PMC: 2011 Dec 16.
Published in final edited form as: Vaccine. 2010 Sep 15;29(2):357–362. doi: 10.1016/j.vaccine.2010.08.099

Figure 1. TNFα and IFNγ contribute to the increased survival mediated by mAb specific for F1 or LcrV after pulmonary exposure to fully virulent pgm-positive Y. pestis.

Figure 1

Wild-type C57BL/6 mice were infected intranasally with 12 LD-50 Y. pestis strain CO92. (A) The following day, they received intraperitoneal injections of PBS or the indicated doses of LcrV- or F1-specific mAb (n= 10 mice/group). In a subsequent study, the infected mice received (B) PBS vehicle control, (C) 15 ug LcrV-specific mAb, (D) 7.5 ug LcrV-specific mAb, (E) 400 µg F1-specific mAb, or (F) 200 µg F1-specific mAb. This time, the injections also included neutralizing mAb specific for the cytokines TNFα and IFNγ (anti-Cytokine; open symbols) or isotype-matched control mAb (Control; closed symbols). In comparison with mice treated with control mAb, mice treated with suboptimal LcrV or F1-specific mAb along with cytokine-neutralizing mAb (D and F, respectively) exhibited significantly reduced survival (both p<0.0001 by Log rank test; n = 10 mice per group).