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. 1998 Nov 2;188(9):1611–1619. doi: 10.1084/jem.188.9.1611

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CTL-mediated peritoneal tumor rejection is normal in B6.TNF⁰ mice. B6, B6.P⁰, and B6.TNF⁰ mice were immunized twice (2 wk apart) with E7 peptide and their spleen cells harvested 1 wk later and stimulated in vitro (as described in Materials and Methods). 5 d after stimulation, the CTL activity of responder cells was determined in a 4-h ⁵¹Cr-release assay (at E/T ratios indicated) using labeled RMA-E7 target cells, RMA-S pulsed with E7^49–57 peptide, or RMA-S pulsed with OVA^257–264. The spontaneous release of ⁵¹Cr was <15%, and the experiment was performed using triplicate samples. (B) Untreated B6, B6.P⁰, and B6.TNF⁰ mice (n = 5/group) or those immunized as above were challenged intraperitoneally 1 wk after the second immunization with 10⁵ RMA-E7 tumor cells in 0.2 ml PBS. Mice were observed daily for tumor growth for up to 70 d by monitoring body weight and development of ascites in mice. Individual mice are represented by each symbol.

CTL-mediated peritoneal tumor rejection is normal in B6.TNF⁰ mice. B6, B6.P⁰, and B6.TNF⁰ mice were immunized twice (2 wk apart) with E7 peptide and their spleen cells harvested 1 wk later and stimulated in vitro (as described in Materials and Methods). 5 d after stimulation, the CTL activity of responder cells was determined in a 4-h ⁵¹Cr-release assay (at E/T ratios indicated) using labeled RMA-E7 target cells, RMA-S pulsed with E7^49–57 peptide, or RMA-S pulsed with OVA^257–264. The spontaneous release of ⁵¹Cr was <15%, and the experiment was performed using triplicate samples. (B) Untreated B6, B6.P⁰, and B6.TNF⁰ mice (n = 5/group) or those immunized as above were challenged intraperitoneally 1 wk after the second immunization with 10⁵ RMA-E7 tumor cells in 0.2 ml PBS. Mice were observed daily for tumor growth for up to 70 d by monitoring body weight and development of ascites in mice. Individual mice are represented by each symbol.