Figure 2.

Early DEX treatment SR-GVHD murine BMT models. (A) Our criteria of steroid responsiveness in murine BMT models. (B–G) B6 WT animals received 10 Gy on day −1 and were transplanted with 3.0 × 10⁶ CD90.2⁺ splenic T cells along with 5 × 10⁶ TCD-BM from either syngeneic B6 or allogeneic MHC matched multiple miHAs mismatched C3H.sw donors. Recipient animals were treated intraperitoneally with 0.1 mg/kg/day of dexamethasone (DEX) from day +7 thru +21 after allo-BMT. (B) Survival. The allogeneic DEX treated animals shown in Fig. 1B were divided into three groups based on our criteria, such as steroid responsive (Res), stable (St) or steroid refractory (Ref) GVHD. n = 3–25 per group. Data shown are pooled from four independent experiments. ***p < 0.001, when Ref animals were compared to other groups. (C) Representative picture of skin response to DEX. (D–G) Histopathological GVHD score in skin (D), liver (E), gastrointestinal (GI) tract (F), and lung (G) on day 14 of DEX treatment (day 21 after allo-BMT) from the different groups in B (n = 3–18 per group). Data are pooled from five independent experiments. *p < 0.05, **p < 0.01. (H) B6D2F1 animals received 11 Gy on day −1 and were transplanted with 3.0 × 10⁶ CD90.2⁺ splenic T cells along with 5 × 10⁶ TCD-BM from either syngeneic B6D2F1 or allogeneic MHC mismatched haploidentical B6 donors. Recipient animals were treated intraperitoneally with 0.1 mg/kg/day of DEX from day +7 thru +21 after allo-BMT. Survival is shown (n = 2–11 per group). Data are pooled from two independent experiments. *p < 0.05, when Ref animals were compared to other groups. Error bars show the mean ± SEM.