中國醫(yī)學(xué)科學(xué)院基礎(chǔ)醫(yī)學(xué)研究所趙春華教授有關(guān)樹突狀細(xì)胞的研究以封面文章形式發(fā)表于血液學(xué)領(lǐng)域權(quán)威雜志《血液》（Blood）上。
本次在Blood上發(fā)表的文章首次將間充質(zhì)干細(xì)胞與樹突狀細(xì)胞的成熟分化命運(yùn)轉(zhuǎn)歸聯(lián)系起來,，尤其是探討了間充質(zhì)干細(xì)胞是否會(huì)影響成熟的樹突狀細(xì)胞的表型（細(xì)胞的外在表現(xiàn)特性）和功能及凋亡,。
研究小組將間充質(zhì)干細(xì)胞和成熟的樹突狀細(xì)胞進(jìn)行共培養(yǎng)（在體外條件下讓它們共同生長(zhǎng)繁殖），結(jié)果證明間充質(zhì)干細(xì)胞不但阻止樹突狀細(xì)胞凋亡，且促使成熟樹突狀細(xì)胞的大量增殖，表型也發(fā)生了改變，即使之成為一種短樹突狀圓型的樹突狀細(xì)胞,，稱之為調(diào)節(jié)性樹突狀細(xì)胞，這種細(xì)胞可存活較長(zhǎng)時(shí)間,，具有較強(qiáng)的吞噬能力,，較高的免疫調(diào)節(jié)活性，同時(shí)免疫原性降低,。
進(jìn)而課題組還深入研究發(fā)生這些改變的分子免疫學(xué)機(jī)制,。研究揭示了間充質(zhì)干細(xì)胞臨床應(yīng)用可預(yù)防治療器官移植中的排斥反應(yīng)以及治療自身免疫性疾病的相關(guān)作用機(jī)制。
趙春華教授的研究受到科技部863計(jì)劃和基金委的長(zhǎng)期支持,。（生物谷Bioon.com）
生物谷推薦原始出處：
Blood, 1 January 2009, Vol. 113, No. 1, pp. 46-57.
Mesenchymal stem cells induce mature dendritic cells into a novel Jagged-2–dependent regulatory dendritic cell population
Bin Zhang1,*, Rui Liu1,*, Dan Shi1, Xingxia Liu1, Yuan Chen1, Xiaowei Dou1, Xishan Zhu1, Chunhua Lu1, Wei Liang1, Lianming Liao1, Martin Zenke2, and Robert C. H. Zhao1
1 Center of Excellence in Tissue Engineering, Department of Cell Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking union Medical College, Beijing, China; and 2 Institute for Biomedical Engineering, Department of Cell Biology, Rheinisch-Westfaelische Technische Hochschule (RWTH) Aachen University Medical School, Aachen, Germany
Mesenchymal stem cells (MSCs), in addition to their multilineage differentiation, exert immunomodulatory effects on immune cells, even dendritic cells (DCs). However, whether they influence the destiny of full mature DCs (maDCs) remains controversial. Here we report that MSCs vigorously promote proliferation of maDCs, significantly reduce their expression of Ia, CD11c, CD80, CD86, and CD40 while increasing CD11b expression. Interestingly, though these phenotypes clearly suggest their skew to immature status, bacterial lipopolysaccharide (LPS) stimulation could not reverse this trend. Moreover, high endocytosic capacity, low immunogenicity, and strong immunoregulatory function of MSC-treated maDCs (MSC-DCs) were also observed. Furthermore we found that MSCs, partly via cell-cell contact, drive maDCs to differentiate into a novel Jagged-2–dependent regulatory DC population and escape their apoptotic fate. These results further support the role of MSCs in preventing rejection in organ transplantation and treatment of autoimmune disease.
