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1 lls presumably due to thymic toxicity of the graft-versus-host reaction.
2 enesis of systemic sclerosis by initiating a graft-versus-host reaction.
3 ly considered to be a minor component of the graft-versus-host reaction.
4 mmune deficiency, cytoreductive regimen, and graft-versus-host reactions.
5 tibodies active against tissue DC to control graft-versus-host reactions.
6 or separating the graft-versus-leukemia from graft-versus-host reactions.
8 ess the roles of these cells in engraftment, graft versus host reactions and graft-host tolerance in
9 anufactured with this process do not mediate graft-versus-host reactions and are rendered resistant t
10 ted donor CD4+ T cells, arising during acute graft-versus-host reactions, are key contributors to the
13 tricted alloreactive T cell responses during graft-versus-host reaction, but failed to control autoim
14 roach to find out whether lymphohaemopoietic graft-versus-host reactions could occur without excessiv
15 ting, the occurrence of subclinical forms of graft-versus-host reaction (GVHR) can seldom be formally
16 ic competitor attenuated the course of acute graft-versus-host reaction in a murine F(1) transfer sem
17 , thymic emigrants failed to induce an acute graft-versus-host reaction in allogeneic severe combined
18 protein 70 (hsp70) in an in vitro-generated graft-versus-host reaction in human skin, using streptav
20 s due to augmentation of lymphohematopoietic graft-versus-host reaction (LGVHR) and can be avoided by
23 immunity, elimination of immune-suppressing graft-versus-host reactions permits superior immune reco
26 understanding and improved management of the graft-versus-host reaction should allow improved prevent
27 d not inhibit donor T cell infiltration into graft-versus-host reaction target organs, but decreased
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