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Sökning: onr:"swepub:oai:gup.ub.gu.se/330506" > Ultra-high static m...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003789naa a2200565 4500
001oai:gup.ub.gu.se/330506
003SwePub
008240528s2023 | |||||||||||000 ||eng|
0247 a https://gup.ub.gu.se/publication/3305062 URI
0247 a https://doi.org/10.1002/mco2.3792 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Gu, H.4 aut
2451 0a Ultra-high static magnetic fields cause immunosuppression through disrupting B-cell peripheral differentiation and negatively regulating BCR signaling
264 1c 2023
520 a 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.image.
650 7a NATURVETENSKAPx Biologix Biokemi och molekylärbiologi0 (SwePub)106022 hsv//swe
650 7a NATURAL SCIENCESx Biological Sciencesx Biochemistry and Molecular Biology0 (SwePub)106022 hsv//eng
653 a metabolism
653 a activation
653 a exposure
653 a glucose
653 a system
653 a serum
653 a wasp
653 a Research & Experimental Medicine
7001 a Fu, Y. F.4 aut
7001 a Yu, B.4 aut
7001 a Luo, L.4 aut
7001 a Kang, D. Q.4 aut
7001 a Xie, M. M.4 aut
7001 a Jing, Y. K.4 aut
7001 a Chen, Q. Y.4 aut
7001 a Zhang, X.4 aut
7001 a Lai, J.4 aut
7001 a Guan, F.4 aut
7001 a Forsman, Huameiu Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning,Institute of Medicine, Department of Rheumatology and Inflammation Research4 aut0 (Swepub:gu)xfuhuv
7001 a Shi, J. M.4 aut
7001 a Yang, L.4 aut
7001 a Lei, J. H.4 aut
7001 a Du, X. R.4 aut
7001 a Zhang, X.4 aut
7001 a Liu, C. H.4 aut
7102 a Göteborgs universitetb Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning4 org
7730 t Medcommg 4:5q 4:5
8564 8u https://gup.ub.gu.se/publication/330506
8564 8u https://doi.org/10.1002/mco2.379

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