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. 2007 Oct 26;57(5):701–718. doi: 10.1007/s00262-007-0410-4

Fig. 5.

Fig. 5

a Reversion of the immunological eclipse mediated by dexamethasone (DX) as evidenced by the restoration of the capacity of mice bearing a large MC-C tumor to restrain the growth of a secondary MC-C tumor implant (concomitant immunity). The figure shows the volume of the secondary tumor (ordinate) as a function of the days after the secondary tumor implant (abscissa). Mice bearing a s.c. MC-C tumor 1,500–2,000 mm3 tumor size, which had received DX 3 days earlier, were challenged with a secondary s.c. implant of 5 × 105 MC-C tumor cells in the contralateral flank (eclipse + DX, n = 14). Untreated tumor bearing mice (eclipse, n = 16) as well as untreated (control, n = 16) and DX-treated normal mice (control + DX, n = 10) challenged with 5 × 105 MC-C tumor cells served as controls. Growth of secondary tumor implant was also determined in tumor-bearing mice which received DX plus the glucocorticoid antagonist RU-486 (eclipse + DX + RU; n = 3) or DX plus anti-CD3 antibody (eclipse + DX + anti-CD3, n = 6). Comparison of Eclipse + DX with the other groups: Day 11: P < 0.01 versus eclipse and control + DX; P < 0.001 versus control and eclipse + DX + RU; P < 0.02 versus eclipse + DX + anti-CD3. Day 16: P < 0.001 versus all the other groups. Day 20: P < 0.01 versus control; P < 0.002 versus eclipse and control + DX; P < 0.001 versus eclipse + DX + anti-CD3 and eclipse + DX + RU. b Reversion of the immunological eclipse mediated by dexamethasone (eclipse + DX), indomethacin (eclipse + indo) and tumor necrosis factor receptor (eclipse + TNFR) as evidenced by the restoration of the capacity of mice bearing a large MC-C tumor (1,500–2,000 mm3) to restrain the growth of a secondary tumor s.c. implant of 5 × 105 MC-C tumor cells in the contralateral flank (concomitant immunity). Control group was represented by normal mice challenged with a s.c. implant of 5 × 105 MC-C tumor cells. The figure shows the volume of the secondary tumor (ordinate) as a function of the days after the secondary tumor implant (abscissa). Comparison between eclipse + DX versus control: day 11: P < 0.01; day 16: P < 0.001; day 20: P < 0.002. Comparison between eclipse + DX versus eclipse + TNFR: days 11, 16 and 20: P < 0.01. Comparison between Eclipse + DX versus eclipse + indo; day 20: P < 0.05. Comparison between eclipse + TNFR and eclipse + indo versus control: days 16 and 20: P < 0.05. c Secondary MC-C tumor challenge prevented to grow in a dexamethasone-treated mice bearing a large primary MC-C tumor (day 25 after secondary tumor implant). Note a dense lymphocyte infiltration (L) followed by a dense fibrotic area (F) surrounding a tumor core (T) (H–E, ×100). d Magnification of c showing an immunological reaction with abundant mononuclear host cells infiltrating the tumor (HE, ×400). e Secondary MC-C tumor challenge growing in untreated mice bearing a large primary MC-C tumor (day 25 after secondary tumor implant). See viable tumor cells displaying mitosis and without lymphocyte infiltration (H–E, ×400)