Fig. 1.
Fig. 1. Mortality and body weight during acute GVHD after allo-BMT. (A) Lethal GVHD was induced by transfer of B6 BM cells plus 2.5 × 107 spleen cells (B6 BMS) into lethally irradiated BDF1 mice. Recipients of B6 BM cells (B6 BM), B6 T-cell–depleted BM cells (B6 TCD-BM), or syngeneic BDF1 BM cells plus spleen cells (BDF1 BMS) manifested no signs of GVHD and almost all recipients survived more than 80 days, except for 1 recipient of B6 BM. (B and C) Contribution of TNF--, FasL-, and perforin-mediated cytotoxic pathways to lethal acute GVHD. Lethally irradiated BDF1 mice were transplanted with BM cells plus 2.5 × 107 spleen cells from wild-type B6 (B6 BMS), B6-gld (gld BMS), or perforin-deficient (PKO BMS) mice. In another group, B6 BMS recipients were administered with anti–TNF- MoAb (B6 BMS + anti–TNF-). Mortality (B) and body weight (C) were monitored at the indicated days after BMT. Administration of anti–TNF- MoAb to the B6 BMS almost completely ameliorated the mortality and the body weight loss resulted from acute GVHD. Survival of the gld BMS and PKO BMS recipients was 100% and 80%, respectively, on day 80 after BMT. The data represent the results of three similar experiments.

Mortality and body weight during acute GVHD after allo-BMT. (A) Lethal GVHD was induced by transfer of B6 BM cells plus 2.5 × 107 spleen cells (B6 BMS) into lethally irradiated BDF1 mice. Recipients of B6 BM cells (B6 BM), B6 T-cell–depleted BM cells (B6 TCD-BM), or syngeneic BDF1 BM cells plus spleen cells (BDF1 BMS) manifested no signs of GVHD and almost all recipients survived more than 80 days, except for 1 recipient of B6 BM. (B and C) Contribution of TNF--, FasL-, and perforin-mediated cytotoxic pathways to lethal acute GVHD. Lethally irradiated BDF1 mice were transplanted with BM cells plus 2.5 × 107 spleen cells from wild-type B6 (B6 BMS), B6-gld (gld BMS), or perforin-deficient (PKO BMS) mice. In another group, B6 BMS recipients were administered with anti–TNF- MoAb (B6 BMS + anti–TNF-). Mortality (B) and body weight (C) were monitored at the indicated days after BMT. Administration of anti–TNF- MoAb to the B6 BMS almost completely ameliorated the mortality and the body weight loss resulted from acute GVHD. Survival of the gld BMS and PKO BMS recipients was 100% and 80%, respectively, on day 80 after BMT. The data represent the results of three similar experiments.

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