Differential rates of replacement of human dermal dendritic cells and macrophages during hematopoietic stem cell transplantation.
Differential rates of replacement of human dermal dendritic cells and macrophages during hematopoietic stem cell transplantation.
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DOI：
10.1084/jem.20081633
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发表时间：
2009-02-16
期刊：
影响因子：
--
通讯作者：
Collin M
中科院分区：
文献类型：
--
作者：
Haniffa M;Ginhoux F;Wang XN;Bigley V;Abel M;Dimmick I;Bullock S;Grisotto M;Booth T;Taub P;Hilkens C;Merad M;Collin M
造血干细胞移植的动物模型已用于分析骨髓衍生的细胞的营业额，并证明受体抗原抗原细胞（APC）在人类与宿主疾病（GVHD）中的关键作用（APC）。髓样衍生的组织APC的谱系关系还没有完全理解。某些受体APC CD1A+和CD14+ DC迅速耗尽并被供体细胞所取代，但是受体巨噬细胞可以在GVHD病变中发现，并且可能持续数月。从正常的真皮促炎细胞因子中分离出来，尽管它们刺激了幼稚或记忆CD4+ T细胞的增殖，但巨噬细胞在记忆中诱导了细胞因子的表达，而CD4+ T细胞的激活和激活和DC细胞的增殖表明。独特的谱系和持续的接受者巨噬细胞虽然不太可能引发同种异体性，但可能有助于通过维持先前激活的T细胞的响应，GVHD。
Animal models of hematopoietic stem cell transplantation have been used to analyze the turnover of bone marrow–derived cells and to demonstrate the critical role of recipient antigen-presenting cells (APC) in graft versus host disease (GVHD). In humans, the phenotype and lineage relationships of myeloid-derived tissue APC remain incompletely understood. It has also been proposed that the risk of acute GVHD, which extends over many months, is related to the protracted survival of certain recipient APC. Human dermis contains three principal subsets of CD45+HLA-DR+ cells: CD1a+CD14− DC, CD1a−CD14+ DC, and CD1a−CD14+FXIIIa+ macrophages. In vitro, each subset has characteristic properties. After transplantation, both CD1a+ and CD14+ DC are rapidly depleted and replaced by donor cells, but recipient macrophages can be found in GVHD lesions and may persist for many months. Macrophages isolated from normal dermis secrete proinflammatory cytokines. Although they stimulate little proliferation of naive or memory CD4+ T cells, macrophages induce cytokine expression in memory CD4+ T cells and activation and proliferation of CD8+ T cells. These observations suggest that dermal macrophages and DC are from distinct lineages and that persistent recipient macrophages, although unlikely to initiate alloreactivity, may contribute to GVHD by sustaining the responses of previously activated T cells.
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