Figure 1
Figure 1. Perforin and Fas in the interactions between T cells and DCs. (A) Activated wild-type (WT) or perforin−/− CD8+ OVA-specific OT1 T cells were incubated with CFSE-labeled WT or Fas-deficient lpr DCs pulsed with OVASIINFEKL peptide. Killing of DCs were quantified with WT versus perforin−/− (mean ± SD): **P < .01 (n = 3). (B) WT or Fas-deficient lpr DCs were pulsed with OVA223-239 peptide and labeled with CFSE. Activated WT or perforin−/− CD4+ OVA-specific OT2 T cells were incubated with DCs. Killing of DCs was quantified (mean ± SD). WT versus perforin−/−: *P < .05, **P < .01 (n = 3). (C) WT or perforin−/− OT1 T cells were injected into recipient mice, followed by injection of CFSE-labeled WT of Fas−/− DCs pulsed with OVASIINFEKL peptide. Draining lymph nodes were harvested. Total cell numbers were counted and percentages of CFSE+ DCs were quantified by flow cytometry. Total CFSE+ DCs were determined (mean ± SD). **P < .01 (n = 5). (D) WT or perforin−/− OT2 T cells were injected into recipient mice, followed by injection of CFSE-labeled WT of Fas−/− DCs pulsed with OVA223-239 peptide. Draining lymph nodes were harvested and total CFSE+ DCs were determined as in (C). *P < .05, **P < .01 (n = 5). (E) Spleen and inguinal lymph nodes were harvested from 6-week-old WT, perforin−/−, DC-Fas−/−, and perforin−/−DC-Fas−/− mice. The weight of spleens of 6-week-old WT, perforin−/−, DC-Fas−/−, and perforin−/−DC-Fas−/− mice was also determined. WT versus perforin−/−DC-Fas−/−: P < .01. (F) Percentages of survival of WT, perforin−/−, DC-Fas−/−, and perforin−/−DC-Fas−/− mice at different ages (n = 20).

Perforin and Fas in the interactions between T cells and DCs. (A) Activated wild-type (WT) or perforin−/− CD8+ OVA-specific OT1 T cells were incubated with CFSE-labeled WT or Fas-deficient lpr DCs pulsed with OVASIINFEKL peptide. Killing of DCs were quantified with WT versus perforin−/− (mean ± SD): **P < .01 (n = 3). (B) WT or Fas-deficient lpr DCs were pulsed with OVA223-239 peptide and labeled with CFSE. Activated WT or perforin−/− CD4+ OVA-specific OT2 T cells were incubated with DCs. Killing of DCs was quantified (mean ± SD). WT versus perforin−/−: *P < .05, **P < .01 (n = 3). (C) WT or perforin−/− OT1 T cells were injected into recipient mice, followed by injection of CFSE-labeled WT of Fas−/− DCs pulsed with OVASIINFEKL peptide. Draining lymph nodes were harvested. Total cell numbers were counted and percentages of CFSE+ DCs were quantified by flow cytometry. Total CFSE+ DCs were determined (mean ± SD). **P < .01 (n = 5). (D) WT or perforin−/− OT2 T cells were injected into recipient mice, followed by injection of CFSE-labeled WT of Fas−/− DCs pulsed with OVA223-239 peptide. Draining lymph nodes were harvested and total CFSE+ DCs were determined as in (C). *P < .05, **P < .01 (n = 5). (E) Spleen and inguinal lymph nodes were harvested from 6-week-old WT, perforin−/−, DC-Fas−/−, and perforin−/−DC-Fas−/− mice. The weight of spleens of 6-week-old WT, perforin−/−, DC-Fas−/−, and perforin−/−DC-Fas−/− mice was also determined. WT versus perforin−/−DC-Fas−/−: P < .01. (F) Percentages of survival of WT, perforin−/−, DC-Fas−/−, and perforin−/−DC-Fas−/− mice at different ages (n = 20).

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