Lack of MZMs increases apoptotic cell–induced proinflammatory cytokines and enhances T-cell responsiveness to apoptotic cell–associated antigens. Eight- to 12-week-old female B6 mice were injected intravenously with 167 μg of CLs or an equivalent amount of PBSLs in a 200-μL final volume. Forty-eight hours later 5 × 10⁷ apoptotic thymocytes were transferred intravenously. (A) Four and 18 hours after thymocyte injection serum was collected and assessed for the presence of IL-6, IL-12, IFN-γ, IL-10, IL-13, TNF-α, TGF-β1, and IL-17. Bars are mean values for 4 mice/group. CL and PBSL control groups are shown for the 18-hour time point. (B) Eight- to 12-week-old female B6.CD45.1 mice were injected intravenously with 167 μg of CLs or an equivalent amount of PBSLs in a 200-μL final volume. Forty-eight hours later 5 × 10⁶ CFSE-labeled splenocytes from CD45.2⁺ OTII mice were transferred intravenously into CL0 and PBSL-treated animals. One day (ie, 24 hours) later 10⁷ apoptotic thymocytes from OVA protein-expressing Act-mOVA mice were transferred by tail vein injection. Three days after apoptotic cell injection single-cell splenocyte suspensions were examined by FACS for the proliferation of the OTII CD4⁺ T cells by virtue of CFSE diminution. Dot plots represent samples gated on the CD4⁺ splenocyte population and stained with antibodies against CD45.2, identifying the transferred OTII CD4⁺ T cells (n = 5 mice/group). (C) Graphic representation of the data presented in panel C. Bars in graphs represent the mean value for 5 mice ± SD; *P < .05 and **P < .01 as determined by the unpaired Student t test. ND indicates none detected. These experiments were repeated at least twice with similar results.