Ultra-high static magnetic fields cause immunosuppression through disrupting B-cell peripheral differentiation and negatively regulating BCR signaling.

Ultra-high static magnetic fields cause immunosuppression through disrupting B-cell peripheral differentiation and negatively regulating BCR signaling.
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DOI:
10.1002/mco2.379
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发表时间:
2023-10
期刊:
影响因子:
9.9
通讯作者:
Liu, Chaohong
Liu, Chaohong
中科院分区:
其他
文献类型:
--
作者:
Gu, Heng;Fu, Yufan;Yu, Biao;Luo, Li;Kang, Danqing;Xie, Miaomiao;Jing, Yukai;Chen, Qiuyue;Zhang, Xin;Lai, Juan;Guan, Fei;Forsman, Huamei;Shi, Junming;Yang, Lu;Lei, Jiahui;Du, Xingrong;Zhang, Xin;Liu, Chaohong

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为提高成像分辨率和检测能力,在过去几十年里,磁共振成像(MRI)中静磁场(SMF)的场强显著提升。然而,关于高磁场副作用的研究仍十分匮乏,且1特斯拉(T)以上静磁场对B细胞的影响从未有过报道。在此,我们发现,暴露于33.0 T的超高静磁场会导致免疫抑制,并扰乱B细胞的分化和信号传导。33.0 T静磁场处理导致B细胞外周分化和抗体分泌紊乱,B细胞膜上IgM的表达减少,且这些影响可能与场强相关。此外,暴露于33.0 T静磁场的小鼠,其B细胞早期激活受到抑制,包括B细胞铺展、B细胞受体聚集和信号体募集,BCR近端信号传导中的正负调节分子均受抑制,肌动蛋白重组也受损。测序和基因富集分析表明,静磁场刺激还会影响脾脏B细胞的转录组和代谢途径。因此,在MRI的临床应用中,我们应考虑静磁场对免疫系统的影响,并选择最佳场强用于治疗。 33.0 T静磁场处理导致B细胞外周分化和抗体分泌紊乱,而较低磁场,包括28.7 T、17.8 T或11.2 T静磁场,产生的此类影响要小得多或无此影响。33.0 T静磁场处理诱导BCR近端信号下调,并损害与F - 肌动蛋白重塑相关的BCR聚集。静磁场刺激会影响B细胞的转录组和代谢途径。
To increase the imaging resolution and detection capability, the field strength of static magnetic fields (SMFs) in magnetic resonance imaging (MRI) has significantly increased in the past few decades. However, research on the side effects of high magnetic field is still very inadequate and the effects of SMF above 1 T (Tesla) on B cells have never been reported. Here, we show that 33.0 T ultra‐high SMF exposure causes immunosuppression and disrupts B cell differentiation and signaling. 33.0 T SMF treatment resulted in disturbance of B cell peripheral differentiation and antibody secretion and reduced the expression of IgM on B cell membrane, and these might be intensity dependent. In addition, mice exposed to 33.0 T SMF showed inhibition on early activation of B cells, including B cell spreading, B cell receptor clustering and signalosome recruitment, and depression of both positive and negative molecules in the proximal BCR signaling, as well as impaired actin reorganization. Sequencing and gene enrichment analysis showed that SMF stimulation also affects splenic B cells' transcriptome and metabolic pathways. Therefore, in the clinical application of MRI, we should consider the influence of SMF on the immune system and choose the optimal intensity for treatment. 33.0 T SMF treatment resulted in disturbance of B cell peripheral differentiation and antibody secretion, but lower magnetic fields, including 28.7, 17.8, or the 11.2 T SMFs had much less or no such effects. 33.0 T SMF treatment induced downregulate BCR proximal signaling and impaired F‐actin remodeling related BCR clustering. SMF stimulation affected the transcriptome and metabolic pathways of B cells. .
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