2010
DOI: 10.1111/j.1537-2995.2009.02440.x
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Immunomonitoring of graft‐versus‐host minor histocompatibility antigen correlates with graft‐versus‐host disease and absence of relapse after graft

Abstract: Our results provide a robust method to monitor mH antigen graft-versus-host reaction and suggest that current identified mH have predictive value on GVHD and GVL.

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Cited by 10 publications
(5 citation statements)
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“…The minor histocompatibility antigens, e.g., HA-1, are immunogenic allogeneic antigens responsible for graft-versus-host disease (GVHD) in HLA-matched bone marrow transplantation ( Tseng et al., 1999 , Voogt et al., 1988 ). Laurin et al. (2010) previously showed that minor histocompatibility antigen-associated alloreactivity plays a critical role in the development of GVHD and graft-versus-leukemia (GVL) after HLA-identical hematopoietic stem cell transplantation.…”
Section: Discussionmentioning
confidence: 99%
“…The minor histocompatibility antigens, e.g., HA-1, are immunogenic allogeneic antigens responsible for graft-versus-host disease (GVHD) in HLA-matched bone marrow transplantation ( Tseng et al., 1999 , Voogt et al., 1988 ). Laurin et al. (2010) previously showed that minor histocompatibility antigen-associated alloreactivity plays a critical role in the development of GVHD and graft-versus-leukemia (GVL) after HLA-identical hematopoietic stem cell transplantation.…”
Section: Discussionmentioning
confidence: 99%
“…In patients transplanted for management of hematological malignancy treatment failure is often attributable to either the development of life--threatening GVHD or the lack of graft versus malignancy (GVM) effects [11,12]. These are, in turn influenced by the immune reconstitution following transplantation [13,14,15,16]. Hypothetically, repertoire complexity emerging in the reconstituting cell populations may be driven, in part, by the disparity in minor histocompatibility antigens encountered in each instance of SCT [17,18].…”
Section: Introductionmentioning
confidence: 99%
“…It has long been postulated that the contingent of cells induced to death includes T-cells associated to the pathology treated. Yet only 5-10% of blood mononuclear cells are exposed to the process (representing less than 1% of the body total T lymphocytes) and only a very small number are the neoplastic T-cell clones or even less in case of GVHD because patients are lymphopenic [4]. Considering the delayed clinical responses observed, mechanisms other than the central role of depleting pathogenic T-cell clones may exist.…”
Section: Mechanisms Of Action For Ecp: From T Lymphocytes Apoptosis Tmentioning
confidence: 97%