Impaired plasma cell differentiation associates with increased oxidative 
metabolism in IkappaBNS-deficient B cells

Erikson, E.; Adori, M.; Khoenkhoen, S.; Zhang, J.; Rorbach, J.; Castro Dopico, X.; Karlsson Hedestam, G.

doi:10.1016/j.cellimm.2022.104516

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Impaired plasma cell differentiation associates with increased oxidative metabolism in IkappaBNS-deficient B cells

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Rorbach, J.
Rorbach – Mitochondrial Gene Expression, External and Associated Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/35413621
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Citation

Erikson, E., Adori, M., Khoenkhoen, S., Zhang, J., Rorbach, J., Castro Dopico, X., et al. (2022). Impaired plasma cell differentiation associates with increased oxidative metabolism in IkappaBNS-deficient B cells. Cell Immunol, 375, 104516. doi:10.1016/j.cellimm.2022.104516.

Cite as: https://hdl.handle.net/21.11116/0000-000B-BAC7-3

Abstract

Mutations causing loss of the NF-kappaB regulator IkappaBNS, result in impaired development of innate-like B cells and defective plasma cell (PC) differentiation. Since productive PC differentiation requires B cell metabolic reprogramming, we sought to investigate processes important for this transition using the bumble mouse strain, deficient for IkappaBNS. We report that LPS-activated bumble B cells exhibited elevated mTOR activation levels, mitochondrial accumulation, increased OXPHOS and mROS production, along with a reduced capacity for autophagy, compared to wildtype B cells. Overall, our results demonstrate that PC differentiation in the absence of IkappaBNS is characterized by excessive activation during early rounds of B cell division, increased mitochondrial metabolism and decreased autophagic capacity, thus improving our understanding of the role of IkappaBNS in PC differentiation.