SOCS1 Regulates the Immunomodulatory Roles of MSCs on B Cells

• Published in: International journal of stem cells 2020-07, Vol.13 (2), p.237-245
• Main Authors: Zhang, Lei, Qu, Yan-Nv, Zhang, He-Yang, Wu, Zhen-Yang, Li, Zhong-Li, Guo, Wan-Bei, Wang, Qi-Ben, Fang, Nan-Zhu, Jiang, Xiao-Xia
• Format: Article
• Language: English
• Subjects: Original
• ISSN: 2005-3606; 2005-5447
• DOI: 10.15283/ijsc20001

The effective use of MSCs for the treatment of some B cell-mediated immune diseases is quite limited. The main reason is that the immunomodulatory effects of mesenchymal stem cells (MSCs) on B cells are unclear, and their underlying mechanisms have not been fully explored. By co-culturing B cells with MSCs without (MSC/CTLsh) or with suppressor of cytokine signaling 1 (SOCS1) knockdown (MSC/SOCS1sh), we found that MSCs inhibited B cell proliferation, activation and terminal differentiation. Remarkably, the highest inhibition of B cell proliferation was observed in MSC/SOCS1sh co-culture. Besides, MSC/SOCS1sh reversed the inhibitory effect of MSCs in the last stage of B cell differentiation. However, MSC/SOCS1sh had no effect on inhibiting B cell activation by MSCs. We also showed that IgA B cell production was significantly higher in MSC/SOCS1sh than in MSC/CTLsh, although no difference was observed when both MSCs co-cultures were compared to isolated B cells. In addition, MSCs increased PGE2 production after TNF- /IFN- stimulation, with the highest increase observed in MSC/SOCS1sh co-culture. Our results highlighted the role of SOCS1 as an important new mediator in the regulation of B cell function by MSCs. Therefore, these data may help to develop new treatments for B cell-mediated immune diseases.