Figure 1.
Figure 1. Establishment of a purified cell model of GVHD. Lethally irradiated B6D2F1 recipients reconstituted with B6-derived HSCs (n = 8) or with HSCs plus 200 000 αβTCR+ splenocytes from B6 donors (n = 14) were assessed for evidence of acute GVHD. Mean ± SE clinical GVHD scores are displayed for each week after BMT. The recipients of HSCs alone showed no clinical GVHD. In contrast, recipients of 2000 HSC + 200 000 αβTCR+ donor TSP exhibited severe and often lethal GVHD, with the peak severity and incidence occurring at week 3 (P = .0005 vs HSCs alone).

Establishment of a purified cell model of GVHD. Lethally irradiated B6D2F1 recipients reconstituted with B6-derived HSCs (n = 8) or with HSCs plus 200 000 αβTCR+ splenocytes from B6 donors (n = 14) were assessed for evidence of acute GVHD. Mean ± SE clinical GVHD scores are displayed for each week after BMT. The recipients of HSCs alone showed no clinical GVHD. In contrast, recipients of 2000 HSC + 200 000 αβTCR+ donor TSP exhibited severe and often lethal GVHD, with the peak severity and incidence occurring at week 3 (P = .0005 vs HSCs alone).

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