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The implications of myelodysplastic syndrome – associated chromosomal abnormalities in the development of graft‐versus‐host disease
Author(s) -
Arai Yasuyuki,
Yamashita Kouhei,
Mizugishi Kiyomi,
TakaoriKondo Akifumi,
Chiba Tsutomu,
Watanabe Tomohiro
Publication year - 2013
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/ejh.12100
Subject(s) - trisomy , cytokine , graft versus host disease , immunology , myelodysplastic syndromes , medicine , transplantation , trisomy 8 , bone marrow , stem cell , disease , pathology , biology , cytogenetics , chromosome , biochemistry , genetics , gene
There is a growing body of evidences that acquired chromosomal abnormalities in bone marrow ( BM ) cells are associated with clinical manifestations of myelodysplastic syndrome ( MDS ). However, to our knowledge, there are no reports that describe the association between chromosomal abnormalities in MDS and graft‐versus‐host disease ( GVHD ) after allogeneic stem cell transplantation (allo‐ SCT ). Here, we describe two MDS cases with trisomy 8 and der(1;7)(q10;p10), who developed severe GVHD after allo‐ SCT . We analyzed cytokine production and cell survival of monocytes from these patients with MDS before allo‐ SCT , in comparison with healthy controls or an MDS patient with a different chromosomal abnormality, who has not developed GVHD . The monocytes from MDS patients with trisomy 8 and der(1;7)(q10;p10) produced a larger amount of pro‐inflammatory cytokine, tumor necrosis factor‐α, and a smaller amount of anti‐inflammatory cytokine, interleukin‐10, on stimulation with Toll‐like receptor ( TLR ) ligands. In addition, the monocytes from MDS cases with GVHD showed a decrease in apoptotic cell death upon stimulation with TLR ligands. We also detected host‐derived pro‐inflammatory antigen‐presenting cells ( APC s) in skin GVHD lesions after allo‐ SCT . These data suggest that trisomy 8 and der(1;7)(q10;p10) may be associated with the development of severe GVHD , by prolonging survival of pro‐inflammatory host‐derived APC s in GVHD lesions.