Summary:Graft-versus-host disease (GVHD) is a major cause of mortality and morbidity after allogeneic bone marrow transplantation, but can be avoided by removing T lymphocytes from the donor bone marrow. However, T cell depletion increases the risk of graft rejection. In this study, two strategies are used to overcome rejection: (1) use of high doses of stem cells obtained from peripheral blood (PBSC), (2) admixture with a CD52 monoclonal antibody in order to deplete both donor and residual recipient lymphocytes. Two antibodies are compared: CAMPATH-1G (rat IgG2b) and its humanized equivalent CAMPATH-1H (human IgG1). A total of 187 consecutive patients at six centers received PBSC transplants from HLA-matched siblings between 1997 and 1999. A wide spectrum of diseases, both malignant and non-malignant, was included. The recovery of CD34 + cells after antibody treatment was close to 100%. The risk of acute GVHD (grade 2 to 4) was 11% in the CAMPATH-1G group and 4% in the CAMPATH-1H group (P = NS). The risk of chronic GVHD (any grade) was 11% in the CAMPATH-1G group and 24% in the CAMPATH-1H group (P = 0.03) but the risk of extensive chronic GVHD was only 2%. The overall risk of graft failure/rejection was 2%, not significantly different between the two antibodies. Antibody treatment was equally effective at concentrations between 10 g/ml and 120 g/ml and it made no significant difference to the outcome whether the patients received post-transplant immunosuppression or not (87% did not). Transplant-related mortality in this heterogenous group of patients (including high-risk and advanced disease) was 22% at 12 months. It is proposed that treatment of peripheral blood stem cells with CAMPATH-1H is a simple and effective method for depleting T cells which may be applicable to both autologous and allogeneic

We studied the outcome of individuals with aplastic anaemia (AA) who received reduced-intensity conditioning followed by the infusion of stem cell grafts that had been T-cell depleted ex vivo with alemtuzumab. Consecutive patients with AA who had an HLA-identical sibling received conditioning with fludarabine 30 mg/m 2 daily for 5 days followed by CY 60 mg/kg on 2 consecutive days. Cytokine-mobilized blood grafts were incubated ex vivo with alemtuzumab 'in the bag' and infused without washing. CYA was prescribed until day þ 90. Engraftment rate, GVHD, EFS and overall survival were studied. Fifteen patients received PBPC grafts. It was the second graft in one of the patients. Ten patients were male and their median age was 23.5 years. The toxicity of the conditioning was minimal. One patient received 1 Â 10 7 /kg donor lymphocytes for rising chimerism. At a median of 1107 (294-1778) days, all of them survived with normal blood parameters. None of them developed acute or chronic GVHD. In patients with AA the combination of purine analogue and alkylator leads to rapid engraftment despite T-cell depletion of grafts. This strategy of reduced-intensity conditioning has low toxicity, does not compromise engraftment and seems effective for prevention of GVHD.