Nakamura, M., Kishi, M., Sakaki, T., Ha- shimoto, H., Nakase, H., Shimada, K., Ishida, E. & Konishi, N. (2003) Novel tu- mor suppressor loci on 6q22-23 in primary central nervous system lymphomas. Cancer Research, 63, 737–741. O’ Neill, B.P., Wang, C.H., O’ Fallon, J.R., Colgan, J.D., Earle, J.D., Krigel, R.L., Brown, L.D. & McGinnis, W.L. (1999) Primary central nervous system non- hodgkin’s lymphoma (PCNSL): survival advantages with combined initial therapy? A final report of the North Central Cancer Treatment Group (NCCTG) Study 86-72- 52. International Journal of Radiation Oncology, Biology, and Physics, 43, 559–563. Xu, Y., Tan, L.J., Grachtchouk, V., Voorhees, J.J. & Fisher, G.J. (2005) Receptor-type protein-tyrosine phosphatase-kappa regu- lates epidermal growth factor receptor function. Journal of Biology Chemistry, 280, 42694–42700. Nakamura, M., Kishi, M., Sakaki, T., Ha- shimoto, H., Nakase, H., Shimada, K., Ishida, E. & Konishi, N. (2003) Novel tu- mor suppressor loci on 6q22-23 in primary central nervous system lymphomas. Cancer Research, 63, 737–741. O’ Neill, B.P., Wang, C.H., O’ Fallon, J.R., Colgan, J.D., Earle, J.D., Krigel, R.L., Brown, L.D. & McGinnis, W.L. (1999) Primary central nervous system non- hodgkin’s lymphoma (PCNSL): survival advantages with combined initial therapy? A final report of the North Central Cancer Treatment Group (NCCTG) Study 86-72- 52. International Journal of Radiation Oncology, Biology, and Physics, 43, 559–563. Xu, Y., Tan, L.J., Grachtchouk, V., Voorhees, J.J. & Fisher, G.J. (2005) Receptor-type protein-tyrosine phosphatase-kappa regu- lates epidermal growth factor receptor function. Journal of Biology Chemistry, 280, 42694–42700. Third-party virus-specific T cells eradicate adenoviraemia but trigger bystander graft-versus-host disease The adoptive transfer of T cells with anti-viral properties against pathogens, such as cytomegalovirus (CMV) and Epstein–Barr virus (EBV), from allogeneic donors to recipients has been shown to be highly effective, both as prophylaxis and treatment for viral reactivation following haematopoietic stem cell transplantation (HSCT) (Rooney et al, 1998; Peggs et al, 2003; Leen et al, 2009). Conventional procedures for the generation of virus-specific T cells require weeks of cell culture and most studies have therefore relied on the elective production and pre-emptive transfer of cells. Recently, tri-specific donor T cell populations with specificity against EBV, CMV and adenovirus (ADV) have been used in this manner (Leen et al, 2006). As an elective strategy this approach is highly effective, but is very labour intensive, time consuming and costly. An alternative approach, which allows rapid identification and enrichment of virus-specific donor cells, relies on the detection of gamma-interferon- (IFN-c) responses to pathogens following ex-vivo stimulation and offers more targeted therapy. A bi-specific antibody is used to ‘capture and fix’ IFN-c as it is released from stimulated cells and magnetic bead selection bead is then used to isolate responding cells (Chatziandreou et al, 2006). The IFN-c capture strategy allows rapid selection of both CD4 + and CD8 + T cells and has recently been tested in pilot studies in the UK (Mackinnon et al, 2008) and Germany (Feuchtinger et al, 2006). We recently deployed this technology to identify and select virus-specific T cells from a third-party donor to treat intractable ADV viraemia following mis-matched unrelated donor stem cell transplantation. The patient, a 7-year-old girl who had suffered relapse of acute lymphoblastic leukaemia (ALL) 2 years after successful treatment with regimen A of the UK-ALL 2003 protocol, had undergone a 1C-mismatched unrelated donor peripheral blood HSCT. She received conditioning with total body irradiation (1440 cGy), cyclophosphamide (200 mg/kg) and alemtuzemab (1 mg/kg). Graft-versus-host disease (GVHD) prophylaxis had ADV SBR Haplo ADV-T cells CD4 10 7 10 8 1000 1200 0·8 10 5 10 6 600 800 umol/l 0·4 0·6 10 4 Copies/ml 200 400 0·2 Cells x10 9 /l 0 50 100 150 10 3 0 Days after SCT 0·0 200 Fig 1. The Adenoviral load is shown peaking at levels above 10 7 /ml and remained grossly elevated despite withdrawal of immunosuppression and Cidofovir therapy. The patient was profoundly lymphopenic, with barely detectable CD4 T cells for the first 100 d. Third party, haploidentical Adenovirus (ADV) T cells were administered on day 104 at a dose of 10 4 /kg, and over the next 4–6 weeks there was clearance of ADV in the peripheral blood. During this period there was also a rapid rise in T cell number and the patient developed skin GVHD (stage III) and liver GVHD (stage IV) with profound cholestasis and grossly elevated serum biluribin (SBR). Correspondence 150 ª 2011 Blackwell Publishing Ltd, British Journal of Haematology, 154, 141–155