Figure 4
Figure 4. LN and PP deficient LTβRIg/TNFRIg-treated recipients develop GVHD. LN- and PP-deficient BALB/c recipients were created by treating pregnant mothers with LTβRIg and TNFRIg. On day 0, WT or LN/PP-deficient (LTβRIg/TNFRIg) recipients received 750 cGy and 9 × 106 BM cells with or without 1.3 × 106 CD4+CD25− cells from B6.C donors. (A) Survival curve. †P < .05 for BM controls versus CD4→WT or CD4→LTBRIg/TNFRIg. Two BM control mice were killed at day 17 because of extensive weight loss (> 30% of original weight), but there was no histologic evidence of GVHD in these animals. (B) Liver, colon, and skin histopathology. P < .05 for BM controls versus CD4→WT or CD4→LTβRIg/TNFRIg for all analyses; *P < .05 for CD4→WT versus CD4→LTβRIg/TNFRIg. NS indicates not significant for CD4→WT versus CD4→LTβRIg/TNFRIg.

LN and PP deficient LTβRIg/TNFRIg-treated recipients develop GVHD. LN- and PP-deficient BALB/c recipients were created by treating pregnant mothers with LTβRIg and TNFRIg. On day 0, WT or LN/PP-deficient (LTβRIg/TNFRIg) recipients received 750 cGy and 9 × 106 BM cells with or without 1.3 × 106 CD4+CD25 cells from B6.C donors. (A) Survival curve. †P < .05 for BM controls versus CD4→WT or CD4→LTBRIg/TNFRIg. Two BM control mice were killed at day 17 because of extensive weight loss (> 30% of original weight), but there was no histologic evidence of GVHD in these animals. (B) Liver, colon, and skin histopathology. P < .05 for BM controls versus CD4→WT or CD4→LTβRIg/TNFRIg for all analyses; *P < .05 for CD4→WT versus CD4→LTβRIg/TNFRIg. NS indicates not significant for CD4→WT versus CD4→LTβRIg/TNFRIg.

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