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Updated: Oct 2, 2026

In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients
Published on: August 12, 2017
Transplantation of T-lymphocyte depleted marrow with an addback of T cells
1University Department of Haematology, Royal Liverpool University Hospital, U.K.
Depletion of T-lymphocytes from allogeneic marrow prior to transplantation decreases the risk of serious graft versus host disease (GvHD), but also increases the risk of relapse. We have used a partial T-cell depletion technique, in the hope of controlling GvHD without compromising relapse risk. Allogeneic marrow was fully T-cell depleted ex vivo with Campath 1M, and infused together with an 'addback' of 2 x 10(5) donor peripheral blood T-cells/kg in 16 consecutive patients undergoing BMT from HLA-identical family members. Post-transplant immunosuppression was with cyclosporin A in conventional dosage. Eight cases developed grade I or II GvHD, limited to the skin in all cases. Only the two grade II cases required steroid therapy; the remainder were easily controlled with simple emollients. No cases of more advanced GvHD were seen. All patients engrafted promptly. With a median follow-up for the survivors of 976 days, seven cases have relapsed, with an overall projected actuarial disease-free survival of 37.5 per cent at 36 months. The overall outcome (good control of GvHD but high relapse rate) is therefore similar to that expected in patients receiving fully T-depleted marrow without post-transplant immunosuppression.
Depletion of T-lymphocytes from allogeneic marrow prior to transplantation decreases the risk of serious graft versus host disease (GvHD), but also increases the risk of relapse. We have used a partial T-cell depletion technique, in the hope of controlling GvHD without compromising relapse risk. Allogeneic marrow was fully T-cell depleted ex vivo with Campath 1M, and infused together with an 'addback' of 2 x 10(5) donor peripheral blood T-cells/kg in 16 consecutive patients undergoing BMT from HLA-identical family members. Post-transplant immunosuppression was with cyclosporin A in conventional dosage. Eight cases developed grade I or II GvHD, limited to the skin in all cases. Only the two grade II cases required steroid therapy; the remainder were easily controlled with simple emollients. No cases of more advanced GvHD were seen. All patients engrafted promptly. With a median follow-up for the survivors of 976 days, seven cases have relapsed, with an overall projected actuarial disease-free survival of 37.5 per cent at 36 months. The overall outcome (good control of GvHD but high relapse rate) is therefore similar to that expected in patients receiving fully T-depleted marrow without post-transplant immunosuppression.
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