We also assessed the role of Ceacam1 in allo-BMT recipients. In our model systems, WT T cells in a Ceacam1-deficient environment showed a phenotype similar to that of Ceacam1 2/2 alloactivated T cells: both showed increased activation, selective damage to the large intestines, and preferential accumulation in the MLN and intestinal parenchyma of mice with GVHD, and correspondingly decreased infiltration of the liver and PLN, ultimately leading to exacerbation of disease, with accelerated mortality in the first two weeks post-transplant. This suggests that Ceacam1 on donor T cells interacts with recipient tissues, and that Ceacam1 ''fraternal'' interactions between cells of the donor graft, were not sufficient to restrain GVHD in Ceacam1 2/2 recipients. However, the increased early mortality of Ceacam1 2/2 allo-BMT recipients with GVHD also led us to ask whether Ceacam1 2/2 mice were sensitive to radiation injury. While Ceacam1 2/2 mice were not significantly defective for hematopoiesis after sublethal irradiation at 3.5 and 4.5 Gy (data not shown), they did exhibit significantly increased damage to the small intestines after lethal irradiation ( Figure 4) .