Figure 2.
Figure 2. TACI-Fc treatment restores CTL expansion in B-cell–deficient mice. B-cell–deficient mice (2 per group) were pretreated with either TACI-Fc or B7RP-1–Fc fusion proteins (1 μg/mouse, intraperitoneally, 24 hours before and 48 hours after peptide priming) then immunized with the VSV NP 52-59 peptide in IFA. Untreated wild-type C57/BL6 mice were also immunized as a control. Mice were killed 7 days after immunization, their spleens were harvested and homogenized into a single-cell suspension, then analyzed ex vivo for peptide-specific IFNγ-producing cells by the ELISPOT assay (A) and for cytolytic activity following additional in vitro stimulation of primed splenocytes with peptide (B). An average of 2 experiments is shown with SD ranging from ≤ 3 (A) and ≤ 4 (B) at all E/T ratios tested.

TACI-Fc treatment restores CTL expansion in B-cell–deficient mice. B-cell–deficient mice (2 per group) were pretreated with either TACI-Fc or B7RP-1–Fc fusion proteins (1 μg/mouse, intraperitoneally, 24 hours before and 48 hours after peptide priming) then immunized with the VSV NP 52-59 peptide in IFA. Untreated wild-type C57/BL6 mice were also immunized as a control. Mice were killed 7 days after immunization, their spleens were harvested and homogenized into a single-cell suspension, then analyzed ex vivo for peptide-specific IFNγ-producing cells by the ELISPOT assay (A) and for cytolytic activity following additional in vitro stimulation of primed splenocytes with peptide (B). An average of 2 experiments is shown with SD ranging from ≤ 3 (A) and ≤ 4 (B) at all E/T ratios tested.

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