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pubmed-article:1525605pubmed:dateCreated1992-10-22lld:pubmed
pubmed-article:1525605pubmed:abstractTextDespite major advances, graft-versus-host disease (GVHD) remains a major obstacle to clinical bone marrow transplantation. Prophylaxis by T cell depletion is associated with increased rates of engraftment failure and leukemic relapse. Treatment with high-dose IL-2 can markedly protect lethally irradiated mice from GVHD-related mortality, especially when T cell-depleted (TCD) syngeneic bone marrow cells (BMC) are co-administered. In these IL-2-protected animals, allogeneic reconstitution is observed, and a graft-versus-leukemia effect of allogeneic T cells is preserved. To determine whether IL-2 might increase alloresistance under conditions in which alloengraftment is more difficult to achieve, we have now evaluated the possible effect of IL-2 on: (1) competitive repopulation of lethally irradiated mice by mixtures of TCD allogeneic and TCD syngeneic BMC; (2) radiation protection by TCD allogeneic BMC; (3) timing of hematologic recovery; and (4) allogeneic engraftment in sublethally irradiated recipients. The results show that IL-2 has only a limited and strain-restricted effect on alloengraftment. This effect may reflect activation of alloresistant host natural killer cells, a cell population which is not essential for the protective effect of IL-2 against GVHD.lld:pubmed
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pubmed-article:1525605pubmed:pagination157-63lld:pubmed
pubmed-article:1525605pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:1525605pubmed:year1992lld:pubmed
pubmed-article:1525605pubmed:articleTitleAlloengraftment in IL-2-treated mice.lld:pubmed
pubmed-article:1525605pubmed:affiliationTransplantation Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown 02129.lld:pubmed
pubmed-article:1525605pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1525605pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
pubmed-article:1525605pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed