CD14+单核细胞旁分泌IL-1β刺激产生的IL-6不参与人脐带间充质干细胞的免疫抑制活性
CD14+单核细胞旁分泌IL-1β刺激产生的IL-6通过激活JNK和NF-κB信号途径，使HUCMSC分泌的IL-6显著增加。阻滞PGE2的合成不影响IL-6的分泌。抗IL-6抗体不能逆转HUCMSC介导的对CD4+T淋巴细胞的抑制。IL-6不参与IL-1β-HUCMSC-PGE2对CD4+淋巴细胞的抑制活性。
延伸：对MSC细胞因子的研究，可能有助于发现新的因子或老因子的新作用。对新药开发有启示作用。
Cell Physiol Biochem. 2012;29(3-4):551-60. doi: 10.1159/000338509. Epub 2012 Apr 3.
IL-6 production stimulated by CD14(+) monocytes-paracrined IL-1β does not contribute to the immunosuppressive activity of human umbilical cord mesenchymal stem cells.
Wang D, Ji YR, Chen K, Du WT, Yang ZX, Han ZB, Chi Y, Liang L, Bayard F, Han ZC.
Source
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.
Abstract
BACKGROUND/AIMS:
Human umbilical cord mesenchymal stem cells (hUC-MSCs) possess immunosuppressive activities but the mechanisms of such activities are not fully understood. Here, we investigated the role of IL-6, one of the characteristic factors of MSCs, in the immunoregulating effect of hUC-MSCs on CD4(+) T lymphocytes.
METHODS:
The condition media from human peripheral blood mononuclear cells (hPBMCs) or CD14+/- cell were tested if stimulating IL-6 production by hUC-MSCs. The related signaling pathway of IL-6, and the immunosuppressive activity of IL-6 on CD4(+) T lymphocytes were studied.
RESULT:
IL-6 production was dramatically increased by hUC-MSCs when co-culturing with resting or activated hPBMCs. CD14(+) monocytes-paracrined IL-1β promoted the secretion of IL-6 by hUC-MSCs via JNK and NF-κB signaling pathway. Blocking of PGE2 synthesis did not affect the secretion of IL-6, anti-IL-6 antibody was not able to reverse hUC-MSCs-mediated inhibition on CD4(+) T lymphocytes. IL-6 did not mediate the suppressive activity of IL-1β-hUC-MSCs- PGE2 on CD4(+) T cell.
CONCLUSION:
CD14(+) monocytes-paracrined IL-1β promotes IL-6 secretion by hUC-MSCs through activating JNK and NF-κB signaling pathway. However, increased IL-6 production does not contribute to immunosuppressive activity of IL-1β-hUC-MSCs- PGE2 on CD4(+) T cells.
Copyright © 2012 S. Karger AG, Basel.
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