Factors influencing gut GvHD after intensified conditioning with Rhenium 188–labeled anti-CD66 monoclonal antibody

complications and TRM? In contrast to the cohort of Bunjes the majority of our patients suffered from Philadelphia chromosome–positive ALL. Several studies demonstrated a high TRM in patients with this disease.2,3 However, this does not explain the high frequency of acute intestinal GvHD. The second obvious difference was the use of unmanipulated grafts or early incremental T-cell add backs. We therefore assume that the combination of anti-CD66 (a, b, c, e) mAb therapy and early exposure to allogeneic T cells might be the reason for intestinal toxicity. Since anti-CD66 (a, b, c, e) antibodies (clone BW250/183) bind intestinal epithelial cells, radioimmunotherapy might cause tissue damage in the bowel.4 This might also trigger intestinal GvHD. Moreover, the antigen CD66a is expressed on the surface of small intestinal intraepithelial lymphocytes (iIEL).5,6 Via cross fire radiolabeled intraepithelial T-cell binding, mAb might cause additional tissue damage. In summary, allografting without T-cell depletion or with early T-cell add backs after conditioning regimens including 188Re-labeled antiCD66 (a, b, c, e) mAb is associated with a high risk of severe intestinal acute GvHD and a high TRM. We therefore suggest that efficient T-cell depletion is strongly recommended for allogeneic hematopoietic cell grafts after a radioimmunotherapy conditioning with antiCD66 (a, b, c, e) mAb. Furthermore, the anticipated benefit of early T-cell add backs should be weighed out carefully with the risk of severe intestinal GvHD. Stefan A. Klein, Stella Hermann, Christoph F. Dietrich, Dieter Hoelzer, and Hans Martin