Figure 3.
Figure 3. Host cell-derived TNF-α does not significantly contribute to the development of IPS after allogeneic BMT. bm1 donor bone marrow and T cells were given to either lethally irradiated syngeneic (bm1, □), allogeneic wild-type (B6129SF2/J, ▪), or allogeneic TNF-α-/- (B6.129-TnfS6tmGk1,) recipient mice, and lung injury after transplantation was assessed as described in “Materials and methods.” (A) Lung histopathology, (B) BAL fluid cellularity, and (C) BAL fluid TNF-α levels were equivalent in both allogeneic groups and significantly increased compared with syngeneic controls. (D-E) Identical results were also found when using a class II disparate system (bm12 → B6; syngeneic [bm12, □], allogeneic wild-type [B6129SF2/J, ▪], or allogeneic TNF-α-/- [B6.129S6-TnftmGk1, group; *P < .05, □ versus ▪ and.] recipients). Data are presented as mean ± SEM; n = 5 to 8 per

Host cell-derived TNF-α does not significantly contribute to the development of IPS after allogeneic BMT. bm1 donor bone marrow and T cells were given to either lethally irradiated syngeneic (bm1, □), allogeneic wild-type (B6129SF2/J, ▪), or allogeneic TNF-α-/- (B6.129-TnfS6tmGk1,) recipient mice, and lung injury after transplantation was assessed as described in “Materials and methods.” (A) Lung histopathology, (B) BAL fluid cellularity, and (C) BAL fluid TNF-α levels were equivalent in both allogeneic groups and significantly increased compared with syngeneic controls. (D-E) Identical results were also found when using a class II disparate system (bm12 → B6; syngeneic [bm12, □], allogeneic wild-type [B6129SF2/J, ▪], or allogeneic TNF-α-/- [B6.129S6-TnftmGk1, group; *P < .05, □ versus ▪ and.] recipients). Data are presented as mean ± SEM; n = 5 to 8 per

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