Ji Yue Ru, Yang Zhou Xin, Han Zhi-Bo, Meng Lei, Liang Lu, Feng Xiao Ming, Yang Shao Guang, Chi Ying, Chen Dan Dan, Wang You Wei, Han Zhong Chao
The State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union of Medical College, Tianjin, China.
Cell Physiol Biochem. 2012;30(6):1526-37. doi: 10.1159/000343340. Epub 2012 Dec 10.
Mesenchymal stem cells (MSC) play important roles in modulating the activities of T lymphocytes, dendritic cells and natural killer cells. These immunoregulatory properties of MSC suggest their therapeutic potential in autoimmune diseases. However, the effects of MSC on B cells are still poorly understood. The present study was designed to investigate the interaction between MSC and B cells both in vitro and in vivo, and to determine the possible mechanism of action.
The effect of human umbilical cord mesenchymal stem cells (UC-MSC) on proliferation and differentiation of B-cells were characterized in vitro, and we also tested the immunoregulatory properties of mouse bone marrow MSC (BM-MSC) on T cell dependent and independent antibody production in vivo in mice.
Treatment with human UC-MSC resulted in an increase of proliferation, differentiation of B cells into plasma cells and production of antibodies in vitro. Mouse BM-MSC significantly enhanced T cell dependent and independent antibodies production in vivo in mice. PGE2 partially mediated the immunosuppressive activity of human UC-MSC but IL-6 did not regulate this activity.
MSC promote proliferation and differentiation of B cells in vitro and in vivo partially through PGE2 but not IL-6.
间充质干细胞(MSC)在调节T淋巴细胞、树突状细胞和自然杀伤细胞的活性方面发挥着重要作用。MSC的这些免疫调节特性表明它们在自身免疫性疾病中的治疗潜力。然而,MSC对B细胞的影响仍知之甚少。本研究旨在探讨MSC与B细胞在体外和体内的相互作用,并确定其可能的作用机制。
在体外表征人脐带间充质干细胞(UC-MSC)对B细胞增殖和分化的影响,并且我们还在体内测试了小鼠骨髓MSC(BM-MSC)对T细胞依赖性和非依赖性抗体产生的免疫调节特性。
用人UC-MSC处理导致体外B细胞增殖增加、分化为浆细胞以及抗体产生增加。小鼠BM-MSC显著增强了小鼠体内T细胞依赖性和非依赖性抗体的产生。前列腺素E2(PGE2)部分介导了人UC-MSC的免疫抑制活性,但白细胞介素-6(IL-6)不调节这种活性。
MSC在体外和体内部分通过PGE2而非IL-6促进B细胞的增殖和分化。