Adipose tissue-derived mesenchymal stem cells have in vivo immunosuppressive properties applicable for the control of the graft-versus-host disease

被引:531
作者
Yanez, Rosa
Lamana, Maria Luisa
Garcia-Castro, Javier
Colmenero, Isabel
Ramirez, Manuel
Bueren, Juan A.
机构
[1] CIEMAT, Hematopoiesis & Gene Therapy Div, Marcelino Botin Fdn, E-28040 Madrid, Spain
[2] Hosp Nino Jesus, Pediat Hematol & Oncol & Hematopoiet Transplant U, Madrid, Spain
[3] Hosp Nino Jesus, Dept Pathol, Madrid, Spain
关键词
stem cell transplantation; graft-versus-host disease; immunosuppression; mesenchymal stem cells; experimental model; BONE-MARROW TRANSPLANTATION; CORD BLOOD; T-CELLS; PROLIFERATION; LEUKEMIA; LYMPHOCYTES; EXPRESSION; INHIBIT; PHASE; VITRO;
D O I
10.1634/stemcells.2006-0228
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Previous studies have shown the relevance of bone marrow-derived MSCs (BM-MSCs) in controlling graft-versus-host disease (GVHD) after allogeneic transplantation. Since adipose tissue-derived MSCs (Ad-MSCs) may constitute a good alternative to BM-MSCs, we have expanded MSCs derived from human adipose tissue (hAd-MSCs) and mouse adipose tissue (mAd-MSCs), investigated the immunoregulatory properties of these cells, and evaluated their capacity to control GVHD in mice. The phenotype and immunoregulatory properties of expanded hAd-MSCs were similar to those of human BM-MSCs. Moreover, hAd-MSCs inhibited the proliferation and cytokine secretion of human primary T cells in response to mitogens and allogeneic T cells. Similarly, ex vivo expanded mAd-MSCs had an equivalent immunophenotype and exerted immunoregulatory properties similar to those of hAd-MSCs. Moreover, the infusion of mAd-MSCs in mice transplanted with haploidentical hematopoietic grafts controlled the lethal GVHD that occurred in control recipient mice. These findings constitute the first experimental proof that Ad-MSCs can efficiently control the GVHD associated with allogeneic hematopoietic transplantation, opening new perspectives for the clinical use of Ad-MSCs.
引用
收藏
页码:2582 / 2591
页数:10
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