Moreover, recipients of Ceacam1-Tg T cells also had reduced intestinal infiltrates despite similar integrin a 4 b 7 expression, suggesting that Ceacam1 regulates the accumulation of donor T cells in target tissues via multiple mechanisms. Thus, our results on donor lymphocyte infiltrates into GVHD target tissues and secondary lymphoid tissues must be interpreted cautiously, as they must be influenced by T cell proliferation, retention and apoptosis, in addition to trafficking. Although Ceacam1 2/2 and Ceacam1-Tg T cells displayed overall symmetric and opposite phenotypes, we also noted differences. Ceacam1-Tg T cells primarily showed decreased proliferation, whereas Ceacam1 2/2 T cells showed changes in proliferation, but also trafficking and activation. Some of these differences may be due to our models: on WT T cells, Ceacam1 is only briefly and transiently upregulated during activation. Consequently, Ceacam1 2/2 T cells are ''missing'' Ceacam1 only transiently, while Ceacam1-Tg T cells constitutively over-express Ceacam1. Furthermore, while Ceacam1 2/2 T cells are effectively insensitive to all Ceacam1 ligands and interactions, Ceacam1-Tg T cells which over-express the protein may have increased fraternal Ceacam1 interactions with other donor T cells, but may not necessarily experience increased Ceacam1 interactions with donor BM or host hematopoietic and non-hematopoietic components. These differences may explain why their activation and trafficking phenotypes are not directly opposed.