CCL5 production by host cells contributes to GVHD after allo-SCT. B6D2F1 mice received transplants from either syngeneic B6D2F1 (□) or allogeneic B6 donors (■) as described in Figure 1, and serum concentrations of CCL5 were measured by ELISA on days 4 and 7 after SCT (A). Data are presented as means plus or minus SEM; n = 4 to 6 mice per group at each time point; *P < .002. Lethally irradiated CCL5^+/+ Balb/c mice received transplants from either syngeneic (gray dotted line) or allogeneic (—,) B6 donors, and CCL5^−/− Balb/c mice received transplants (– – –) as described in “Materials and methods.” Complete absence of CCL5 in transplant recipient mice results in improved survival after allo-SCT (B). Data are combined from 2 similar experiments; n = 10 to 20 per group; *P < .04 (allo-CCL5^−/− vs allo-CCL5^+/+). CCL5 chimeric balb/c mice (wild-type [WT] → CCL5^−/− [gray solid line] or CCL5^−/− → WT [– – –]) were generated as described in “Materials and methods” and were subsequently used as transplant recipients in the second of 2 tandem experiments. The absence of CCL5 in host APCs also results in a significant survival advantage following allo-SCT. Data are from 1 experiment; n = 4 to 10 per group; **P = .01 (CCL5^−/− → WT vs WT → CCL5^−/−).